Monday, September 25, 2017

Colorado Chronic Wasting Disease CWD TSE Prion Mandatory Submission of test samples in some areas and zoonosis

COLORADO

MANDATORY CHRONIC WASTING DISEASE (CWD) TESTING IN SELECT GMUs... 

To help us gauge the presence of CWD in select deer herds, CPW will require mandatory submission of CWD test samples from some hunter-harvested bucks and does during the 2017 archery, muzzleloader and rifle seasons. Any notified hunter that harvests a deer in the hunts specified in the hunt tables on the following pages will be required to present their deer for testing at a CPW facility. There will be no charge for this mandatory sampling. 



Q3. Does Colorado have CWD? 

A3. Yes. CWD has been found in deer, elk and moose herds in various locations in Colorado. 

About half of Colorado’s deer herds and one-third of our elk herds are known to be infected with CWD. 

A map of locations is included in CPW’s Big Game Brochure, and highlights game management units in red where CWD has been detected: 



see more here;

C OL OR A D O PA R K S & W I L DL I F E

CHRONIC WASTING DISEASE (CWD)

COLORADO PARKS & WILDLIFE • 6060 Broadway, Denver, CO 80216 • 303-297-1192 • cpw.state.co.us

 FREQUENTLY ASKED QUESTIONS

Q1. What is CWD?

A1. Chronic wasting disease (CWD) is a fatal neurological disease found in species of the deer family (“cervids”). It belongs to a family of diseases caused by prions (abnormally shaped proteins). This particular prion attacks the brains of infected deer, elk and moose, causing the animals to display abnormal behavior, become uncoordinated and emaciated, and eventually die.

Q2. What wildlife species are affected by CWD?

A2. All four of the species of the deer family in Colorado are known to be naturally susceptible to CWD: elk, mule deer, white-tailed deer and moose. Natural susceptibility appears to be limited to species that are members of the deer family (cervids) and not pronghorn, bighorn sheep and mountain goat.

Q3. Does Colorado have CWD?

A3. Yes. CWD has been found in deer, elk and moose herds in various locations in Colorado. About half of Colorado’s deer herds and one-third of our elk herds are known to be infected with CWD. A map of locations is included in CPW’s Big Game Brochure, and highlights game management units in red where CWD has been detected: Big Game unit map Q4. Is there a risk to humans?

A4. Disease in humans resulting from CWD exposure has not been reported to date. However, there may be a small risk from eating meat from infected animals. Consequently, public health officials recommend that people avoid exposure to CWD-infected animals. Please see the Colorado Department of Public Health and Environment website (www.colorado.gov/pacific/cdphe/prion-diseases) for the most current recommendations on carcass testing and other preventive measures.

Q5. What CWD precautions and preventative measures should hunters take?

A5. To minimize exposure to CWD and other diseases of potential concern, Colorado Parks and Wildlife (CPW) and state public health officials advise hunters not to shoot, handle or consume any deer, elk or moose that is acting abnormally or appears to be sick. When field-dressing game, wear rubber gloves and minimize the use of a bone saw to cut through the brain or spinal cord (backbone). Minimize contact with brain or spinal cord tissues, eyes, spleen or lymph nodes. Always wash hands and utensils thoroughly after dressing and processing game meat. More information can be found at this website: More CWD Information

A practical CWD video designed for hunters who want to learn and see more can be found here: CWD video

Q6. Why should people be concerned about CWD?

A6. Chronic wasting disease (CWD) poses a significant threat to the future health and vitality of captive and free-ranging mule deer, white-tailed deer, elk and moose populations throughout twenty-six states and provinces in North America. A growing body of evidence suggests that unchecked CWD epidemics can impair the long-term performance of affected populations. The disease shortens the lifespan of infected animals. As a larger proportion of the population becomes infected, older age classes suffer high rates of mortality, and the average age declines. If CWD infection rates are high enough, the population may not be able to sustain itself.

CWD poses serious problems for wildlife management, and the implications for free-ranging deer and elk are significant. Recent studies have shown local declines in deer abundance associated with CWD epidemics, and computer modeling suggests that CWD could substantially reduce deer, elk or moose populations by lowering adult survival rates. Where it occurs, CWD may alter the management of wild deer, elk and moose populations. For example, management recommendations in other states have sharply reduced the density of deer in areas with high CWD infection rates to slow the spread of the disease.

Q7. Why do we want to prevent CWD prevalence rates from increasing in Colorado?

A7. As CWD prevalence rates increase within a specific herd, the likelihood of animals in that herd becoming infected also increases. Older animals have a higher potential for exposure to CWD — particularly for mule deer bucks — and as more of them die from the disease relative to younger animals, the average age of the herd decreases. A proportion of younger animals will also become infected and die at an early age. Animals will begin to die from the disease two years after infection. Considering this information, it is best to prevent high prevalence rates from occurring in a herd. If CWD prevalence is already high, removing older bucks to decrease the sex ratio and achieve a younger age structure before the disease affects the entire herd is a preferred strategy to reduce prevalence.

Q8. What is Colorado doing to manage CWD?

A8. Colorado Parks and Wildlife is currently reassessing when management actions should be taken to control CWD in Colorado’s deer, elk and moose herds. Since it is unlikely that CWD can be eradicated, the overall goal is to prevent CWD from increasing in prevalence or spreading. The primary management approach will use hunter harvest because public hunters are CPW’s best tool to remove infected animals and prevent the spread of CWD. Management actions have previously been taken to reduce CWD prevalence, and the effectiveness has varied.

MANDATORY CWD TESTING

Q9. Why is CPW implementing a mandatory CWD test in 2017? What is the objective?

A9. Voluntary submissions of hunter-harvested deer, elk and moose for CWD testing have been low and limit CPW’s ability to determine infection rates of CWD. As a result, CPW will resume mandatory harvest submissions of mule deer from select Game Management Units in 2017 to increase the number of samples submitted for testing. The objective is to improve CPW’s knowledge of CWD infection rates, which may influence harvest management as well as herd management decisions.

Mandatory CWD testing has been authorized under the CPW Director’s authority in accordance with CPW regulation Chapter W-02.209.F. Mandatory testing occurs periodically in select units, whereas voluntary submissions are accepted annually statewide.

Q10. Why is testing for CWD important?

A10. The proportion of animals in the population that are infected (prevalence rate) is needed to inform wildlife management. Our ability to understand prevalence rates relies on biological samples collected from a large number of animals in a herd.

Q11. What Game Management Units (GMUs) are included in the mandatory sampling effort? Are all hunters licensed for the selected GMUs required to participate in the mandatory sample?

A11. All rifle season buck hunters licensed for Game Management Units (GMUs) 7, 8, 9, 11, 12, 13, 19, 20, 22, 23, 24, 33, 61, 62, 64, 65, 131, 191, 211 and 231 who harvest a buck are required to submit their deer head or have a CWD sample taken. In addition, all deer hunters in GMU 33 who harvest a deer of either sex are required to submit their deer head or have a CWD sample taken.

Q12. Why were some GMUs selected for mandatory CWD testing and not others?

A12. CPW has limited funds to pay for statewide CWD testing, which is why only select GMU were chosen for sampling in 2017.

Q13. Why will the mandatory sampling effort focus on bucks and not does?

A13. There are many reasons why the mandatory testing predominantly includes bucks instead of does. Not all GMUs in the state have doe harvest, whereas all units do have buck harvest. Because of this, there is much higher and more consistent buck harvest statewide, which better supports the assessment of long term trends in prevalence. Also, prevalence rates are generally higher in bucks, so there is a greater chance to find CWD in a herd if resources are focused on testing only bucks. Based on this knowledge, CPW will only be testing bucks in the 2017 mandatory sample with one exception:

GMU 33 is the only unit where all buck and doe hunters were selected for the mandatory sample.

Q14. Is it true that CWD is more common in bucks than does?

A14. In Colorado, yes. CWD studies have shown that prevalence rates for adult bucks are approximately double the prevalence rates found for the adult does of the same population. In addition, older bucks are more likely to have CWD than younger bucks. Thus, a commonly recommended management practice for reducing CWD prevalence rate is to reduce the buck:doe ratio and the average age of bucks.

Q15. Why isn’t CPW including elk or moose in the mandatory CWD testing?

A15. Infection rates are higher in deer than in elk and moose; therefore, the initial focus is on deer. CWD is more likely to cause a population impact in deer because prevalence is generally higher than in elk and moose, making testing a higher priority for deer than for elk and moose.

Q16. How and when will hunters be informed that they are selected for mandatory CWD testing?

A16. Hunters that are selected for mandatory CWD testing will receive a CPW notification letter by mail in August of 2017. CPW strongly encourages hunters to update their contact information registered with the state at: cpw.state. co.us/UpdateInfo

Q17. What does it mean if I receive a letter from CPW notifying me I was selected for mandatory CWD testing?

A17. Anyone who is selected for mandatory CWD testing is required to bring the requested sample (head) of their harvested deer to a CPW Area or Regional Wildlife Office for testing. A list of office locations can be found here. According to CPW regulation Chapter W-02.209.F, it is unlawful to fail to submit CWD samples if you are selected for mandatory CWD testing.

Q18. I was selected for mandatory CWD testing. Where do I need to bring my sample? What part of my deer do I need to bring? What else do I need to bring with me?

A18. You should take the deer head to a CPW Area or Regional Wildlife Office submission site. Specific locations and operating hours of the submission sites can be found here: cpw.state.co.us/CWD-Test What to bring to the CPW submission site:

1. Hunting License. You must bring your hunting license so CPW can obtain the information on your license. If someone else submits your deer head, they must bring a copy of your hunting license or Customer Identification (CID) number, but the carcass tag that came with your license should remain with the carcass.

2. Location of Harvest (GPS coordinates or map location). You will be asked for the GMU, date of harvest and the geographic coordinates (Lat/Long or UTM) of where you harvested your deer. If coordinates are not available, you will be asked to show where the deer was harvested on a map at the submission site.

3. CWD Sample. Please bring only the head of your deer to the submission site as soon as possible, preferably within 5 days of harvest. When removing the head, leave 2 to 4 inches of the neck below the lower jawbone and base of the skull. Whole brains or pieces of brain are not accepted for testing. Please wrap the exposed area with cheese cloth or similar material to prevent tissues from falling out of the skull. Keep the head cool, dry, and avoid freezing if possible. Antlers and capes from harvested deer may be removed by hunters before submitting heads for sampling. CPW will not remove antlers or capes for hunters. CPW suggests that hunters planning shoulder-mount taxidermy should take their animal to the taxidermist before submitting the head for CWD testing. Hunters planning European-mount taxidermy should bring the head to the CPW submission site before the taxidermist and plan to leave the head until a sample can be taken. You may have to wait up to a day to get your head back. Hunters planning taxidermy or mounting should notify CPW personnel at the submission site.

Q19. How soon after harvest do I need to submit my CWD sample for testing?

A19. It is recommended that the head of the harvested animal is submitted for testing as soon as possible. We highly recommend bringing the head to a CPW Area or Regional Wildlife Office submission site within 5 days of harvest. If possible, keep the head cool, dry, and prevent it from freezing until you are able to submit the sample.

Q20. Does the mandatory CWD test cost the hunter anything?

A20. No. Hunters selected for mandatory CWD testing will not have to pay for the test. Q21. If I was not selected for mandatory CWD testing, do I need to pay to test my animal for CWD?

A21. Yes. The service is still available for hunters that wish to test their animal for CWD. Hunters not selected at random for free mandatory CWD testing and wish to have their animal tested will have to pay the subsidized rate of $25.00 for the test. The cost of processing and testing each sample for CWD is approximately $75.00, but CPW is only charging hunters $25.00 to test their animal.

Q22. If I was not selected for mandatory CWD testing, can I volunteer my deer for the sake of science?

A22. Yes, you can, but if you were not selected to receive a free CWD test as part of the mandatory sample, you will need to pay $25.00 for CWD testing. If you submit your deer head for CWD testing, you will be able to access your CWD test results from the CPW website.

Q23. Can I take and submit my own CWD tissue sample?

A23. The collection of the correct tissues for CWD testing requires special training. CPW recommends bringing your deer head to a submission site or to a licensed veterinarian trained to collect the tissue samples needed for testing. If a veterinarian is used, you still need to bring the sample to a CPW submission site.

Q24. How long will it take to receive the test results?

A24. Test results will take a minimum of two weeks and on average three weeks before they are available. During late seasons and times of high volume sample collection, CPW anticipates that test results may take longer than three weeks. Q25. What should I do with the meat while waiting for the CWD test results to come back?

A25. Hunters should process their deer as they normally would while waiting for the CWD test results. If using commercial processing, request that your carcass is processed and packaged separately. Marking packaged meat to clearly identify what animal it represents will aid in distinguishing meat from a CWD-positive animal if the test results are positive.

Q26. What happens if my deer is CWD positive? Am I eligible for a new tag or a refund?

A26. CPW recommends that hunters not eat the meat or tissues of an animal that tests positive for CWD. Refunds or antlerless licenses may be issued in any unit approved by CPW for the same species in the same year to hunters who harvest a deer, elk or moose in which CWD is detected through CPW’s CWD monitoring or testing programs. Please see CPW regulations in Chapter W-16 Article 4 for detailed information regarding refunds and reissued license eligibility resulting from CWD positive test results.

Q27. What are the chances that my deer has CWD?

A27. CPW suggests looking at a recent CWD prevalence map to learn what the infection rate was estimated to be for the area of the state where you hunted your deer. Maps for deer and elk can be found here. Higher prevalence means that there is a higher chance your harvested deer is infected with CWD. For example, <1 100="" 10="" 2017="" 20="" 5-10="" about="" adult="" allow="" and="" animals="" are="" area="" bucks="" collected="" colorado="" contrast="" cpw="" current="" cwd-positive.="" cwd="" deer="" div="" does.="" every="" fellow="" fewer="" for="" from="" generally="" has="" have="" herds.="" hunters="" in="" information="" likely="" mandatory="" map="" means="" more="" of="" older="" one="" out="" positive.="" prevalence="" provide="" s="" sample="" speaking="" submissions="" submitted="" tested="" testing="" than="" that="" the="" this="" to="" update="" voluntary="" will="" with="" you="" younger="" your="">

Q28. If my deer has CWD, what do I do with the meat and carcass?

A28. In the case that a harvested deer tests positive for CWD, the hunter should carefully discard the animal. CPW recommends that all parts of a CWD infected animal, including processed meat, be contained in two heavy duty plastic garbage bags and put out with the weekly trash or brought to the local landfill. Each plastic garbage bag should be independently tied.

CPW will accept donations of unprocessed or processed meat that is infected with CWD for research purposes at the CWD submission sites in Fort Collins, Denver and Craig. Processed meat must not contain spices of any kind to be eligible for a donation.

Q29. How will I learn about the test results?

A29. As soon as results are known, they will be available on the CPW website (cpw.state.co.us/CWD-Test). Remember to save your CWD head tag number, which is needed to look up your results.

ADDITIONAL INFORMATION (CWD)

Q30. Where can I learn more about CWD?

A30. We suggest visiting the following websites:

CPW’s CWD webpage: http://cpw.state.co.us/CWD

The Colorado Department of Public Health and Environment website: 


CWD Alliance webpage: cwd-info.org


In Colorado, some cervids (a group of animals that includes deer, elk and moose) have a prion disease called Chronic Wasting Disease (CWD). Unpublished research from the Canadian Food Inspection Agency has shown that some monkeys that are closely related to people can get CWD from eating meat from infected deer. This means it might be possible for people to get CWD from eating meat from infected animals, but no cases of CWD in people have been found so far. Because of this, if game is harvested in a Game Management Unit (GMU) where CWD has been detected at more than 5%, hunters are encouraged to have the carcass tested for CWD before eating the meat. More information about how to get carcasses tested and where CWD has been detected can be found at the Colorado Parks and Wildlife website: http://cpw.state.co.us/learn/Pages/ResearchCWD.aspx. 
Suspected CJD and other human prion diseases are reportable to public health in Colorado. If you would like to report a case of human prion disease please visit the How to Report a Disease or call the Communicable Diseases Branch at 303-692-2700.
If you have any questions about prion diseases, please call the Communicable Diseases Branch at 303-692-2700 and ask to speak to someone about prion diseases.



2017

Subject: ***CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat










CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat

Chronic Wasting Disease (CWD)

Prevention 

If CWD could spread to people, it would most likely be through eating of infected deer and elk. In a 2006-2007 CDC survey of U.S. residents, nearly 20 percent of those surveyed said they had hunted deer or elk and more than two-thirds said they had eaten venison or elk meat. However, to date, no CWD infections have been reported in people.

Hunters must consider many factors when determining whether to eat meat from deer and elk harvested from areas with CWD, including the level of risk they are willing to accept. Hunters harvesting wild deer and elk from areas with reported CWD should check state wildlife and public health guidance to see whether testing of animals is recommended or required in a given state or region. In areas where CWD is known to be present, CDC recommends that hunters strongly consider having those animals tested before eating the meat.

Tests for CWD are monitoring tools that some state wildlife officials use to look at the rates of CWD in certain animal populations. Testing may not be available in every state, and states may use these tests in different ways. A negative test result does not guarantee that an individual animal is not infected with CWD, but it does make it considerably less likely and may reduce your risk of exposure to CWD.

To be as safe as possible and decrease their potential risk of exposure to CWD, hunters should take the following steps when hunting in areas with CWD:

Do not shoot, handle or eat meat from deer and elk that look sick or are acting strangely or are found dead (road-kill). When field-dressing a deer: Wear latex or rubber gloves when dressing the animal or handling the meat. Minimize how much you handle the organs of the animal, particularly the brain or spinal cord tissues. Do not use household knives or other kitchen utensils for field dressing. Check state wildlife and public health guidance to see whether testing of animals is recommended or required. Recommendations vary by state, but information about testing is available from many state wildlife agencies. Strongly consider having the deer or elk tested for CWD before you eat the meat. If you have your deer or elk commercially processed, consider asking that your animal be processed individually to avoid mixing meat from multiple animals. If your animal tests positive for CWD, do not eat meat from that animal. The U.S. Department of Agriculture’s Animal and Plant Health Inspection Service regulates commercially farmed deer and elk. The agency operates a national CWD herd certification program. As part of the voluntary program, states and individual herd owners agree to meet requirements meant to decrease the risk of CWD in their herds. Privately owned herds that do not participate in the herd certification program may be at increased risk for CWD.

Page last reviewed: August 17, 2017 Page last updated: August 17, 2017 Content source: Centers for Disease Control and Prevention National Center for Emerging and Zoonotic Infectious Diseases (NCEZID) Division of High-Consequence Pathogens and Pathology (DHCPP)


> However, to date, no CWD infections have been reported in people. 

key word here is 'reported'. science has shown that CWD in humans will look like sporadic CJD. SO, how can one assume that CWD has not already transmitted to humans? they can't, and it's as simple as that. from all recorded science to date, CWD has already transmitted to humans, and it's being misdiagnosed as sporadic CJD. ...terry 

LOOKING FOR CWD IN HUMANS AS nvCJD or as an ATYPICAL CJD, LOOKING IN ALL THE WRONG PLACES $$$ 

*** These results would seem to suggest that CWD does indeed have zoonotic potential, at least as judged by the compatibility of CWD prions and their human PrPC target. Furthermore, extrapolation from this simple in vitro assay suggests that if zoonotic CWD occurred, it would most likely effect those of the PRNP codon 129-MM genotype and that the PrPres type would be similar to that found in the most common subtype of sCJD (MM1).***






Molecular Barriers to Zoonotic Transmission of Prions 

*** chronic wasting disease, there was no absolute barrier to conversion of the human prion protein. 

*** Furthermore, the form of human PrPres produced in this in vitro assay when seeded with CWD, resembles that found in the most common human prion disease, namely sCJD of the MM1 subtype.





TUESDAY, SEPTEMBER 12, 2017

CDC Now Recommends Strongly consider having the deer or elk tested for CWD before you eat the meat






2017 PRION CONFERENCE

First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress 

Stefanie Czub1, Walter Schulz-Schaeffer2, Christiane Stahl-Hennig3, Michael Beekes4, Hermann Schaetzl5 and Dirk Motzkus6 1 

University of Calgary Faculty of Veterinary Medicine/Canadian Food Inspection Agency; 2Universitatsklinikum des Saarlandes und Medizinische Fakultat der Universitat des Saarlandes; 3 Deutsches Primaten Zentrum/Goettingen; 4 Robert-Koch-Institut Berlin; 5 University of Calgary Faculty of Veterinary Medicine; 6 presently: Boehringer Ingelheim Veterinary Research Center; previously: Deutsches Primaten Zentrum/Goettingen 

This is a progress report of a project which started in 2009. 21 cynomolgus macaques were challenged with characterized CWD material from white-tailed deer (WTD) or elk by intracerebral (ic), oral, and skin exposure routes. Additional blood transfusion experiments are supposed to assess the CWD contamination risk of human blood product. Challenge materials originated from symptomatic cervids for ic, skin scarification and partially per oral routes (WTD brain). Challenge material for feeding of muscle derived from preclinical WTD and from preclinical macaques for blood transfusion experiments. We have confirmed that the CWD challenge material contained at least two different CWD agents (brain material) as well as CWD prions in muscle-associated nerves. 

Here we present first data on a group of animals either challenged ic with steel wires or per orally and sacrificed with incubation times ranging from 4.5 to 6.9 years at postmortem. Three animals displayed signs of mild clinical disease, including anxiety, apathy, ataxia and/or tremor. In four animals wasting was observed, two of those had confirmed diabetes. All animals have variable signs of prion neuropathology in spinal cords and brains and by supersensitive IHC, reaction was detected in spinal cord segments of all animals. Protein misfolding cyclic amplification (PMCA), real-time quaking-induced conversion (RT-QuiC) and PET-blot assays to further substantiate these findings are on the way, as well as bioassays in bank voles and transgenic mice. 

At present, a total of 10 animals are sacrificed and read-outs are ongoing. Preclinical incubation of the remaining macaques covers a range from 6.4 to 7.10 years. Based on the species barrier and an incubation time of > 5 years for BSE in macaques and about 10 years for scrapie in macaques, we expected an onset of clinical disease beyond 6 years post inoculation. 

PRION 2017 DECIPHERING NEURODEGENERATIVE DISORDERS 

Subject: PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS VIDEO

PRION 2017 CONFERENCE DECIPHERING NEURODEGENERATIVE DISORDERS

*** PRION 2017 CONFERENCE VIDEO



SATURDAY, JULY 29, 2017

Risk Advisory Opinion: Potential Human Health Risks from Chronic Wasting Disease CFIA, PHAC, HC (HPFB and FNIHB), INAC, Parks Canada, ECCC and AAFC



SEE UPDATED SCIENCE ON CWD ZOONOTIC TSE PRION AND THEN THE HISTORY OF CWD TSE PRION IN COLORADO AND VERY POSSIBLY THE ORIGIN OF THE CWD TSE PRION

Friday, April 22, 2016

COLORADO CHRONIC WASTING DISEASE CWD TSE PRION SURVEILLANCE AND TESTING PROGRAM IS MINIMAL AND LIMITED


THURSDAY, FEBRUARY 09, 2012

Colorado Farm-Raised Deer Farms and CWD there from 2012 report Singeltary et al


Sunday, November 13, 2011 

COLORADO CWD CJD TSE PRION REPORTING 2011 


Wasting disease spreads in Colorado Game farm shipped 400 exposed elk to 15 states Hal Herring Nov. 5, 2001 From the print edition PRINT SHARE

 For the past three years, the state of Colorado has required that the brains of all domestic elk that die on elk ranches be tested for chronic wasting disease, a deadly brain malady related to mad cow disease (HCN, 12/18/00: Cure or curse?). In late September, the state's vigilance paid off.

Officials discovered the disease in seven elk herds around the state, the worst outbreak in U.S. history. All but one of the infected elk were quickly traced back to the Elk Echo Ranch, a 2,000-acre breeding and boarding facility near the community of Stoneham in northeastern Colorado.

By the time the state discovered the infections, the Elk Echo had shipped over 400 elk to facilities around Colorado and to 15 other states. The outbreak could have an enormous impact on the region's elk ranching industry - as well as on wild herds of deer and elk - and state officials in Colorado and elsewhere are pulling out all the stops to contain it.

As of mid-October, 1,131 domestic elk and a small herd of captive white-tailed deer were scheduled for destruction in Colorado. The state has purchased a special "air curtain" incinerator, which is supposed to raise temperatures high enough to neutralize the infectious disease agent, to dispose of the carcasses. State officials will transport about 150 live elk to Fort Collins for research on the disease, but the consequences of escape are considered so serious that the animals will be marked with orange paint and accompanied by a truck carrying a marksman with a rifle. New Mexico and Idaho also plan to depopulate herds that include animals traced to the Elk Echo Ranch.

"We're going to wipe out the herds where we've found it, all of them," says Jim Rubing, the chairman of the Captive Wildlife and Alternative Livestock Board at the Colorado Department of Agriculture. "Until we start depopulating, we're not going to know the extent of the problem."

Questions at ground zero

snip...read full article;



COLORADO THE ORIGIN OF CHRONIC WASTING DISEASE CWD TSE PRION?

*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep.
IN CONFIDENCE, REPORT OF AN UNCONVENTIONAL SLOW VIRUS DISEASE IN ANIMALS IN THE USA 1989 http://webarchive.nationalarchives.gov.uk/20080102193705/http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf

ALSO, one of the most, if not the most top TSE Prion God in Science today is Professor Adriano Aguzzi, and he recently commented on just this, on a cwd post on my facebook page August 20 at 1:44pm, quote;

''it pains me to no end to even comtemplate the possibility, but it seems entirely plausible that CWD originated from scientist-made spread of scrapie from sheep to deer in the colorado research facility. If true, a terrible burden for those involved.'' August 20 at 1:44pm ...end


CHRONIC WASTING DISEASE EXPOSURE RISKS FROM COLORADO DIVISION OF WILDLIFE RESEARCH ACTIVITIES

Historical records and interviews have been used to ascertain the potential to which wild cervid populations may have been exposed to chronic wasting disease (CWD) from research activities of the Colorado Division of Wildlife (CDOW) and collaborators that used animals from the CDOW¹s Foothills Wildlife Research Facility (FWRF) in Fort Collins, Colorado. The general principle at FWRF, at least since 1985, has been that deer or elk, once born in, or brought to the facility, do not leave. This was not always true, and the following are summaries of projects where captive animals associated with FWRF could have been placed in contact with wild populations.

Elk Research in Rocky Mountain National Park (RMNP) (Further details appended at the end of this report) ­ Conducted between 1976 and 1978, this study used 5 tame elk obtained from Sybile Wildlife Research Unit in Wyoming and the Denver Zoo. The tame elk grazed freely in selected areas of the park for 75 - minute feeding trials. The total time each animal spent in feeding trials was 260 hours over the 2 years of fieldwork. The tame animals were maintained in a holding pen at Little Horseshoe Park at RMNP in November ­ March and June ­ September both years. The tame animals never were held at FWRF prior to or during the study, but instead were reared and held at holding pens south of the Division offices on Prospect Road, Fort Collins. There is no record of CWD occurrence at these pens.

The tame elk were taken to FWRF after the study in 1978 and, approximately 3 years after they had last been at RMNP, 2 of the animals showed clinical symptoms of CWD and died in 1981. The remaining 3 were euthanized in 1985 (when all cervids at FWRF were killed). CWD was not detected via histopathology.

Elk ­ Cattle Competition Research at Little Snake Wildlife Management Area, ~ 19 mi. north of Maybell, CO (Further details appended at the end of this report)­ Conducted between 1986 and 1990, any potential exposure to CWD would have occurred in the final 2 years, 1989 ­ 1990. Eleven elk captured as calves in RMNP and then reared in chlorine-treated pens at FWRF were used in the study and were returned to FWRF at the end of each field season. 4 of these elk eventually were found to have CWD; the remainder, including 4 that still live, did not contract the disease. One of the CWD elk died at FWRF, between the 1989 and 1990 field seasons. Another died in May 1991, more than 1 year after the study was terminated. The other CWD deaths occurred in June 1992 and February 1995, again at FWRF. These cases are described in Miller et al., 1998.

152 wild elk were also at the Little Snake study facility during the time of potential exposure, and subsequently were released in place, back to the wild. The maximum potential exposure consisted of the potential for nose-to-nose contact between 10 wild elk and from 1 to 4 possible CWD elk (tame) across an electrified fence during two 4.5-month periods. The remaining wild elk had potential exposure from the excreta deposited by tame elk during a single 2-hour grazing trial in each pasture each of two years (4 hours total/pasture). Since not all tame elk entered all pastures, and numbers of wild elk in each pasture varied, the numbers given are the maxima.

Middle Park Deer Studies, Federal Aid Projects W-038-R (Source data are lacking ­ the following information comes from secondary sources, including Federal Aid reports). - The Junction Butte captive animal facility (near Kremmling, CO) and FWRF shared a number of deer during the late 1970s - these deer typically were held at Junction Butte during the summer and at FWRF during the winter. In the period 1975 ­ 1985, at least 2 mule deer at Junction Butte displayed symptoms thought to indicate CWD and died. Other mule deer (5 ­ 7) at Junction Butte displayed similar symptoms and were destroyed at FWRF. In 1976, wild does (number not known) were trapped and held at Junction Butte until fawning. Fawns were transported to FWRF for hand-rearing for research purposes, and the adult does were released into the wild. from September 1985 until March 1991, no animals were held at Junction Butte. From March through September 1991, about 40 confiscated elk and their calves were held at Junction Butte. There is no indication from available surveillance data that CWD infected these elk, or has become established in free-ranging deer associated with Junction Butte. Examinations of 410 harvested mule deer from DAU D-9 (Middle Park) in 1999 did not yield any CWD-positive animals. There is a 98% probability that a CWD-positive animal would have been detected at a prevalence of > 0.01.

Little Hills (Piceance Basin, southwest of Meeker) Studies (Source data are lacking ­ the following information comes from secondary sources) ­ Between 40 and 50 captive deer were moved between FWRF or Colorado State University pens and Little Hills for food habits studies between 1975-1980 (4 deer were from Junction Butte). Typically fawns were obtained at Little Hills, taken to FWRF for hand rearing, and then transported to Little Hills for research. It is not clear whether CWD cases were diagnosed at the Little Hills facility. A report (80W101) on a CWD case from May 1980 includes, as part of the history narrative, a statement that the subject deer was "raised at Little Hills where there has not been a confirmed cases of chronic wasting disease". However, this deer had spent 1 winter at Junction Butte (Kremmling). It is unclear from the report whether this deer died at Little Hills, Kremmling, or Fort Collins; the "Location of origin" is listed as "Meeker (Little Hills) Colorado, Division of Wildlife", but whether that is the ultimate or proximate origin of this deer can¹t be discerned. One tame deer escaped the Little Hills facility in 1979 and another escaped in 1980. Additionally, 2 were lost to predators in the Little Hills facility. The remaining animals were apparently returned to the FWRF. There is no indication from available surveillance data that CWD has become established in free-ranging deer that could have been associated with the Little Hills studies. Examinations of 434 harvested mule deer from DAU D-7 (White River), primarily GMU¹s 22,23,11, and 211 had not yielded any CWD-positive animals prior to 2002. There is a 99% probability that a CWD-positive animal would have been detected at a prevalence of > 0.01.

STUDY DETAILS FROM ROCKY MOUNTAIN NATIONAL PARK and LITTLE SNAKE STATE WILDLIFE AREA (pdf file)

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Subject: CHRONIC WASTING DISEASE UPDATE -- SURVEILLANCE OF WILD ANIMALS 

Date: Fri, 04 Oct 2002 12:13:19 -0700 

From: "Terry S. Singeltary Sr." 

To: BSE-L@uni-karlsruhe.de

CHRONIC WASTING DISEASE UPDATE http://wildlife.state.co.us/cwd/chronicupdate.asp#Exposure_Risks Colorado Division of Wildlife September 30, 2002 Compiled by Jeff Ver Steeg, Terrestrial Section Manager

research/management l captive herd status l regulation issues CWD-related meetings l Federal involvement l recent news Exposure risks from research activities Study Details from Rcky Mtn. Nat. Pk & Little Snake SWA

SURVEILLANCE OF WILD ANIMALS

Ongoing surveillance conducted by the Colorado Division of Wildlife indicates that chronic wasting disease (CWD) is found in wild deer and elk herds in northeastern Colorado and in wild mule deer in a portion of Routt County in the northwest part of the state. Since 1996, the Division, in cooperation with the University of Wyoming and Colorado State University, has examined more than 3,000 animals from throughout the state, including each of the large mule deer herds on the Western Slope. With the exception of the Routt County finding, none have been infected with CWD. In addition to this statewide sampling, the Division also has examined more than 8,500 deer and elk harvested or culled in the CWD-established portions of northeastern Colorado. Estimated infection rates in mule deer harvested from the northeastern CWD-established management units through 2001 range from 0.01

On September 6, 2002 a Division of Wildlife officer shot an elk in Routt County (GMU 441) which later tested positive for CWD, the first time an elk with the disease has been found outside of northeastern Colorado. Following up on a report from an area resident, the officer found the elk in poor condition suffering from an injured jaw. The animal was tested for CWD as part of the agency¹s disease surveillance effort. Two different tests performed at Colorado State University¹s diagnostic laboratory confirmed the elk was infected with CWD.

Detection of CWD in Hunter-Killed Mule Deer in GMU 461

A mule deer buck killed by an archery hunter on Labor Day, just west of Chatfield Reservoir in Jefferson County, tested positive for CWD. This is the furthest south in Colorado an infected animal has been found. The unit is just southwest of Denver and is bordered on one side by the South Platte River. Last winter, a mule deer with CWD was found along the foothills in Jefferson County (GMU 38) about 10 miles south of Boulder. At the time, this was the furthest south an animal with CWD had been found in the state.

CWD Detected in Captive White-tailed Deer in Wisconsin

On September 19, 2002 the Wisconsin State Department of Agriculture, Trade and Consumer Protection was notified that a white-tailed deer on a hunting preserve game farm in Portage County had tested positive for CWD. The State Veterinarian immediately quarantined the farm. State officials learned that the positive deer may have been purchased from a farm in Walworth County. The State Veterinarian quarantined the second farm pending an investigation.

Wisconsin Shooters Collect 539 Deer During Summer Program

On September 17, 2002 the Wisconsin DNR announced that landowners and DNR personnel killed 539 deer within the 389-square mile CWD eradication zone during the fourth and final shooting period of the summer. Final test results are not expected until early November 2002. During the first week-long shooting period (June 8-14), 262 deer were taken. Six of these tested positive for CWD. Of the 336 deer taken during the second period (July 13-19), 7 tested positive. These 7 new cases bring the tally of known CWD cases in the CWD-infection area to 31 animals since the first positives were announced on February 28th. Test results from the third shooting period (August 10-16) are not available yet. One of the positive cases from the second shooting period was sufficiently close to the established eradication zone boundary that the zone will be modified slightly to maintain a 4-mile buffer around all known CWD-positive cases. The addition will add approximately 15 square miles to the existing 374-square mile zone. The DNR remains committed to sampling about 50,000 deer from around the state beginning this fall.

CWD Found in Captive Elk in Minnesota

Minnesota animal-health officials confirmed that state¹s first case of chronic wasting disease on August 30, 2002. The state Board of Animal Health said a farm-raised elk in Aitkin County tested positive after dying mysteriously. The remainder of the herd has been placed under quarantine. Officials are investigating the source of the infection.

CWD Found in Captive Elk in South Dakota

The South Dakota State Veterinarian announced on August 16, 2002 that CWD had been detected in a 3-year old bull elk from a private ranch in Custer County. The discovery was made as result of routine slaughter surveillance. This represents the first case of CWD in captive elk in that state since 1997. An adjacent herd was destroyed 51 months previously due to CWD. The 3-year old bull was from a double-fenced herd, which had been quarantined for 4 years as a precaution due to fence-line contact with the destroyed herd. Following 52 months of surveillance on deaths of all elk 16 months and older with no evidence of disease, the herd was not considered at risk. The elk herd (approximately 140 animals) is under quarantine and will be depopulated.

CWD Found in Wild Mule Deer in New Mexico

The New Mexico Department of Game and Fish announced on June 19. 2002 that a mule deer collected from the White Sands Missile Range tested positive for Chronic Wasting Disease. The Department declared an Animal Health Emergency, closing the state to any importation of deer or elk. Director Larry Bell said the Wyoming State Veterinary Laboratory confirmed the positive test on June 17. This is the first case of CWD in the state of New Mexico.

Suspect Cases in Colorado

The Colorado Division of Wildlife continues to examine cases of suspect animals (deer and elk exhibiting neurological symptoms similar to those seen in advanced cases of CWD). Most recently an animal was collected from near Pagosa Springs. Based on the independent opinions of two expert pathologists, the animal was not afflicted with CWD. Many states are now increasing their efforts to examine such cases.

CWD Found in a Colorado GMU 38

CWD has been found in game management unit 38, immediately west and north of Denver. A single deer was found dead in a yard during the winter of 2001. The animal was likely in the final stages of infection and apparently died of the disease. Test results confirmed the animal was positive for CWD. This is the first time the disease has been found south of Boulder. Unit 38 is directly south of unit 29. The Division also reported finding 3 additional CWD positive deer from unit 29. All 3 were collected as road kills from within the city of Boulder between November and December 2001.

Wildlife Commission Policy on CWD

The Wildlife Commission revised its policy on June 10, 2002. The revision primarily provides the Division additional direction regarding a finding of CWD in areas of the state where the disease was not previously known to exist in wild deer or elk. A copy of the revised policy can be found on the Division¹s website.

Outside Review of Colorado¹s CWD Management Program

The Division of Wildlife began discussing the concept of forming a review panel in October 2001. The discussions were precipitated largely by a recommendation from a few wildlife professionals outside of the Division. Later that fall and winter the Division began to receive similar recommendations from the public. In response to these suggestions, Director Russell George decided to convene such a panel and on March 25, 2001 he extended an invitation to five individuals. The five experts were selected on the basis of their expertise relative to the topic of managing wildlife diseases. All five individuals agreed to serve on the "Blue Ribbon Panel." The Panel was charged with reviewing and evaluating the Division¹s scientific approach to managing CWD in the wild cervid populations of the CWD-established area in northeastern Colorado. The Division specifically asked that the reviewers be critical of any shortcomings or weaknesses they find. The Division also requested feedback on those components of management that the Panel considered reasonable or justified in light of available information.

The Panel met in Denver on May 23-24. At this meeting Panel members were briefed on the topic of CWD in Colorado. A representative of the Panel made a presentation at the national CWD Symposium in August in Denver. The Panel praised the Division¹s management and research efforts thus far and offered suggestions for the future. The Division anticipates a final copy of the Panel¹s report by mid-September 2002.

Discovery of CWD Southeast of Craig, Colorado

During January and February 2002, hunters and Division staff destroyed more than 340 entrapped wild deer and elk at the Motherwell facility in Routt County (on the West slope of Colorado). The animals were killed in order to prevent them from escaping back into the wild after having been inadvertently confined the previous summer with captive-bred elk. On March 29, 2002 the Division of Wildlife announced that one wild mule deer from this facility had tested positive for CWD. A second wild mule deer from the same sample was subsequently diagnosed as having CWD. Beginning April 1, 2002, Division removed 311 wild mule deer within a 5-mile radius of the Motherwell facility. The operation took less than 48 hours. The effort was designed to provide managers with an initial assessment of whether or not the disease was present in free-roaming deer and elk outside the facility. Two of the deer tested positive for CWD, confirming that the disease exists in wild deer on the West slope of Colorado. An additional 18 deer were then killed near the location of the two positive wild deer. Testing of these indicated a third CWD-positive free-roaming deer. During the week of April 15, Division staff (with the able assistance of USDA-APHIS, local landowners and interested constituents) culled approximately 134 elk and 284 deer from within the same 5-mile radius of the Motherwell facility. Final test results indicate a total of 10 positive mule deer (6 from outside of the pens and 4 from inside the pens). All elk have tested negative. During the past four years the Division has tested more than 2000 samples of deer and elk (including more than 400 from herds in the vicinity of the Motherwell elk ranch) from outside of the CWD-established area. Until April 2002, no free-roaming wild animals outside of the CWD-established area in northeastern Colorado had been found to be infected.

State Carcass Importation Restrictions

Several states currently have or are considering carcass transportation recommendations or regulations for this fall. Hunters are advised to contact their state of residence and the state(s) where they intend to hunt to ensure they are aware of the latest information. There is no single convenient source for a nationwide listing of such regulations at this time.

Texas Live Animal Importation Restriction

On March 23, 2002, the Texas Animal Health Commission and the Parks and Wildlife Department issued separate orders that suspended the importation of live white-tailed deer, black-tailed deer, mule deer and elk into Texas to prevent the potential spread of CWD.

Mouse Skeletal Tissue and Prions

An article by Bosque et al. recently published in the Proceedings of the National Academy of Sciences reports that researchers were able to produce pathogenic prions in the skeletal (hind leg) muscle tissue of experimentally inoculated lab mice. The article notes that researchers have not determined whether high levels of aberrant prions can be produced in the skeletal muscle of naturally infected cattle, sheep, elk or deer. The authors also remind readers that oral transmission of prions is inefficient when compared to transmission via inoculation. Previous research completed by Colorado State University and the Division of Wildlife indicated that prions accumulate only in certain parts of infected animals - the brain, eyes, spinal cord, lymph nodes, tonsils, pancrease and spleen. That research also indicated that prions, misshapen proteins that cause the disease, do not accumulate in muscle tissue of affected deer and elk (as determined by immunohistochemistry). Additional tests recently conducted by the University of Wyoming in collaboration with French researchers support the original results. Given no evidence to the contrary, the Division continues to recommend that hunters (1) avoid harvesting obviously sick deer or elk, and (2) bone out the meat and consume only muscle tissue from animals harvested in CWD-established units. Furthermore, public health officials, including the World Health Organization, recommend against eating any animal known to be infected with CWD.

Wisconsin Outbreak in Wild White-tailed Deer

Six new cases of chronic wasting disease have been reported in Wisconsin, prompting officials on August 2, 2002 to widen a special zone west of Madison by nearly 4% in an attempt to eliminate the entire deer population in that area. The latest finding brings the number of deer reported to have contracted CWD to 24, according to the state Department of Natural Resources.

Efforts to eradicate the deer population in the Mount Horeb area, where the 24 deer have tested positive for chronic wasting disease, have yielded 954 white-tailed deer during three one-week hunts. The population of deer in the area has been estimated at about 25,000. The state Department of Natural Resources has scheduled another one-week hunt to begin Sept. 7 to be followed by an extended deer-hunting season. The goals is to halt the spread of the CWD to other parts of Wisconsin and beyond the state's borders.

Prior to July 2002, eighteen white-tailed deer killed by hunters, landowners and agency personnel in south-central Wisconsin had tested positive for CWD. These deer represent the first known cases of the disease in free-roaming deer or elk east of the Mississippi River. An investigation into the source of the outbreak is ongoing. Tests of deer killed by hunters during the 2001 season revealed the first three CWD-positive cases. Landowners and Wisconsin DNR employees acted quickly to cull about 516 white-tailed deer from a 415 square mile area around the first three positive locations in order to determine the extent of the outbreak. All 18 positives were within 13 miles of each other. The 18 positives indicate a prevalence rate of about 3.5% in the focus area. The DNR has announced plans to kill as many as 20,000 deer in a 361-square mile eradication zone in response to the discovery of CWD in wild Wisconsin white-tails.

Alberta Case in Farmed Elk

A single case of CWD has been reported in a farmed elk from Alberta, Canada.

Northeast CWD-established Area of Colorado

In 2002, the Colorado Division of Wildlife documented for the first time positive CWD cases in wild deer in GMUs 87, 88, 89, and 90, all in the tablelands north of the South Platte River. The results are not surprising given that units with positive cases surrounded these units. Prevalence ranges from less than one percent to 5% in these units, but the estimates thus far are based on very small sample sizes.

Nebraska Outbreak in White-tailed Deer

Officials with the Nebraska Game and Parks Commission report the discovery of chronic wasting disease in a confined white-tailed deer herd in northwest Nebraska. Approximately 51% of deer from inside the 800-acre facility have tested positive for wasting disease. Prevalence rates of free-roaming deer tested within a radius of 10 miles from the facility range from 3.4% to 6.8%. White-tailed deer may be more susceptible to the disease than mule deer or elk, and it is possible that the disease spreads more rapidly in the species. Because white-tails tend to be more social than mule deer, it is likely that deer outside the fenced-in area have had nose-to-nose contact with confined deer exposed to the disease. Nebraska officials fear that if the disease is not contained in the wild soon, it will spread further into the free-ranging white-tail population, putting the entire state¹s deer herd at risk.

Testing

In cooperation with the Veterinary Diagnostic Lab of Colorado State University (CSU), the Division of Wildlife is gearing up to collect and test as many as 50,000 hunter harvested deer and elk statewide this fall. Approximately 600 animals (more than 1200 samples) have been tested as of the end of September 2002. The Colorado Department of Agriculture, nearly two dozen members of the Colorado Veterinary Medical Association (CVMA) and many outfitters and guides are also assisting. Hunters desiring testing of deer and elk for CWD can take the heads of harvested animals to approximately 60 locations (Division offices, private veterinarians and "head barrels") throughout Colorado. It is hoped that a new Enzyme Linked Immuno Sorbent Assay (ELISA) screening procedure will allow CSU to process tests in less than a few weeks. Last fall, as an unfortunate result of unusual problems experienced by some cooperating labs, turn around times for tests results took as long as several months in some cases. The Division and those labs chose to delay testing until the reliability of the process was restored. It should be noted that test results are not provided for the purpose of assuring food safety.

Testing is mandatory for hunters taking deer and elk in northeastern Colorado during early, late, regular or private land only (PLO) rifle seasons in GMU's 7, 8, 9, 19, 20, 29, 38, 87, 88, 89, 90, 91, 92, 93, 94, 95, 96, 191, and 951. Therse hunters are required to submit their elk or deer head for CWD sampling within 5 days after harvest. The head must be submitted to one of the locations identified in the mailing sent to these hunters (please see Division¹s website ­ "Hunter Letter 8/02" under the CWD link ­ for details). Successful hunters must complete the special survey tag available at the collection site and attach it to the animal's head. Hunters may remove antlers and capes from harvested elk before submitting heads for sampling. The Division will pay the cost of testing in all cases where testing is mandatory. Hunters not required to participate in the mandatory program (including those early-season archery and muzzleloader hunters in the northeast) may volunteer to have their animals tested. The fee for Division-extracted samples is $17. The fee for sampling by participating CVMA veterinarians is $47.

CHRONIC WASTING DISEASE EXPOSURE RISKS FROM COLORADO DIVISION OF WILDLIFE RESEARCH ACTIVITIES

Historical records and interviews have been used to ascertain the potential to which wild cervid populations may have been exposed to chronic wasting disease (CWD) from research activities of the Colorado Division of Wildlife (CDOW) and collaborators that used animals from the CDOW¹s Foothills Wildlife Research Facility (FWRF) in Fort Collins, Colorado. The general principle at FWRF, at least since 1985, has been that deer or elk, once born in, or brought to the facility, do not leave. This was not always true, and the following are summaries of projects where captive animals associated with FWRF could have been placed in contact with wild populations.

Elk Research in Rocky Mountain National Park (RMNP) (Further details appended at the end of this report) ­ Conducted between 1976 and 1978, this study used 5 tame elk obtained from Sybile Wildlife Research Unit in Wyoming and the Denver Zoo. The tame elk grazed freely in selected areas of the park for 75 - minute feeding trials. The total time each animal spent in feeding trials was 260 hours over the 2 years of fieldwork. The tame animals were maintained in a holding pen at Little Horseshoe Park at RMNP in November ­ March and June ­ September both years. The tame animals never were held at FWRF prior to or during the study, but instead were reared and held at holding pens south of the Division offices on Prospect Road, Fort Collins. There is no record of CWD occurrence at these pens.

The tame elk were taken to FWRF after the study in 1978 and, approximately 3 years after they had last been at RMNP, 2 of the animals showed clinical symptoms of CWD and died in 1981. The remaining 3 were euthanized in 1985 (when all cervids at FWRF were killed). CWD was not detected via histopathology.

Elk ­ Cattle Competition Research at Little Snake Wildlife Management Area, ~ 19 mi. north of Maybell, CO (Further details appended at the end of this report)­ Conducted between 1986 and 1990, any potential exposure to CWD would have occurred in the final 2 years, 1989 ­ 1990. Eleven elk captured as calves in RMNP and then reared in chlorine-treated pens at FWRF were used in the study and were returned to FWRF at the end of each field season. 4 of these elk eventually were found to have CWD; the remainder, including 4 that still live, did not contract the disease. One of the CWD elk died at FWRF, between the 1989 and 1990 field seasons. Another died in May 1991, more than 1 year after the study was terminated. The other CWD deaths occurred in June 1992 and February 1995, again at FWRF. These cases are described in Miller et al., 1998.

152 wild elk were also at the Little Snake study facility during the time of potential exposure, and subsequently were released in place, back to the wild. The maximum potential exposure consisted of the potential for nose-to-nose contact between 10 wild elk and from 1 to 4 possible CWD elk (tame) across an electrified fence during two 4.5-month periods. The remaining wild elk had potential exposure from the excreta deposited by tame elk during a single 2-hour grazing trial in each pasture each of two years (4 hours total/pasture). Since not all tame elk entered all pastures, and numbers of wild elk in each pasture varied, the numbers given are the maxima.

Middle Park Deer Studies, Federal Aid Projects W-038-R (Source data are lacking ­ the following information comes from secondary sources, including Federal Aid reports). - The Junction Butte captive animal facility (near Kremmling, CO) and FWRF shared a number of deer during the late 1970s - these deer typically were held at Junction Butte during the summer and at FWRF during the winter. In the period 1975 ­ 1985, at least 2 mule deer at Junction Butte displayed symptoms thought to indicate CWD and died. Other mule deer (5 ­ 7) at Junction Butte displayed similar symptoms and were destroyed at FWRF. In 1976, wild does (number not known) were trapped and held at Junction Butte until fawning. Fawns were transported to FWRF for hand-rearing for research purposes, and the adult does were released into the wild. from September 1985 until March 1991, no animals were held at Junction Butte. From March through September 1991, about 40 confiscated elk and their calves were held at Junction Butte. There is no indication from available surveillance data that CWD infected these elk, or has become established in free-ranging deer associated with Junction Butte. Examinations of 410 harvested mule deer from DAU D-9 (Middle Park) in 1999 did not yield any CWD-positive animals. There is a 98% probability that a CWD-positive animal would have been detected at a prevalence of > 0.01.

Little Hills (Piceance Basin, southwest of Meeker) Studies (Source data are lacking ­ the following information comes from secondary sources) ­ Between 40 and 50 captive deer were moved between FWRF or Colorado State University pens and Little Hills for food habits studies between 1975-1980 (4 deer were from Junction Butte). Typically fawns were obtained at Little Hills, taken to FWRF for hand rearing, and then transported to Little Hills for research. It is not clear whether CWD cases were diagnosed at the Little Hills facility. A report (80W101) on a CWD case from May 1980 includes, as part of the history narrative, a statement that the subject deer was "raised at Little Hills where there has not been a confirmed cases of chronic wasting disease". However, this deer had spent 1 winter at Junction Butte (Kremmling). It is unclear from the report whether this deer died at Little Hills, Kremmling, or Fort Collins; the "Location of origin" is listed as "Meeker (Little Hills) Colorado, Division of Wildlife", but whether that is the ultimate or proximate origin of this deer can¹t be discerned. One tame deer escaped the Little Hills facility in 1979 and another escaped in 1980. Additionally, 2 were lost to predators in the Little Hills facility. The remaining animals were apparently returned to the FWRF. There is no indication from available surveillance data that CWD has become established in free-ranging deer that could have been associated with the Little Hills studies. Examinations of 434 harvested mule deer from DAU D-7 (White River), primarily GMU¹s 22,23,11, and 211 had not yielded any CWD-positive animals prior to 2002. There is a 99% probability that a CWD-positive animal would have been detected at a prevalence of > 0.01.

STUDY DETAILS FROM ROCKY MOUNTAIN NATIONAL PARK and LITTLE SNAKE STATE WILDLIFE AREA (pdf file)

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This page last updated 09/30/2002

Greetings list members,

some of you may not be familiar with Toms archive of CWD data. some _excellent_ data...


CWD ARCHIVE OLDER ARTICLES



Colorado Policy

27 Jan 99 Dept. of Agriculture Animal Industry Division Colorado Division of Wildlife: -- Ranching for Wildlife See also proposed amended rules Search hunting regs using 'chronic' "The Colorado Department of Agriculture has taken strong preventative measures to protect Colorado's domesticated deer and elk populations from chronic wasting disease, a nervous system disease causing holes in the brain. The Colorado Department of Agriculture passed rules in April 1998 requiring all domesticated deer and elk producers to submit samples from any sick or dying deer or elk to Colorado State University for lab analysis to determine if that animal tests positive for chronic wasting disease (CWD). To date, there have been no positive cases. Chronic wasting disease has been found in approximately five percent of free-roaming deer and less than one percent in free-roaming elk in two small geographic areas in Northcentral Colorado. The agriculture department examines all resident domesticated herd inventories, making sure that free-roaming deer or elk are not incorporated. All deer and elk with CWD in other states have been quarantined and cannot be transported into Colorado. [Does this mean all trace-back and trace-forward herds or only clinically ill animals? -- webmaster] All resident and imported domesticated deer and elk are tattooed; tested for other diseases, then tagged with an official USDA tag. Again, any animal testing positive is not allowed in the state. [There is no test on live animals -- webmaster]The department also requires all domesticated deer and elk to have health certificates, and entry permits to track their movement....

Colorado has a scrapie eradication plan as well adopting a directive at the 71st Annual Convention on June 21, 1998. Recall the first case of scrapie was diagnosed in the United States in sheep originating from Britain via Canada in 1947,. From this initial case until September 30, 1996, scrapie has been diagnosed in 1281 sheep in 850 flocks throughout the U.S.

The Rocky Mountain Regional Animal Health Laboratory offers a free CWD test kit.

Dept of Wildlife Funding: " Unlike most other agencies, the Division receives no tax monies appropriated from the General Tax Fund. Since being directed to do so by the state Legislature in 1921, the Division relies primarily on fees paid for hunting and fishing licenses to pay for its operations.... But the economic benefits to the state are far greater than the income generated by license sales. Hunters and anglers annually inject $1.7 billion into the economy when they purchase the equipment, gas, lodging and other materials in pursuit of their sport....

The Colorado Division of Wildlife receives no state tax money. Instead, the agency is funded by the purchase of fishing and hunting licenses; by federal funds generated by an excise tax on the manufacture of arms, ammunition and other sporting equipment; by donations to the nongame fund and by federal endangered species funds." �

Elk tags were the single largest source of money, providing $27.1 million in 1996-97; deer tags provided a further $11.8 million. These figures represent 49.7% and 21.&% of the entire agency budget. Fishing licenses provided most of the remainder of the total budget of $76.7 million. Non-residents contributed $37.8 million to the total; an elk tag costs $250.

Using game tag receipts and cost of tags, it can be calculated that non-residents purchased 92,000 elk tags while residents purchased 125,000. With deer, non-residents pruchased 65,890 tags; residents purchased 93,827. While not all hunts are successful, not all hunts are in an endemic area, and not all animals harbor CWD, still 376,000 total tags were sold in the 1996-97 season. Pooling of carcasses at game processing facilities both dilutes CWD infectious titre while ensuring that many more hunters get some. The elk population is estimated at 216,000 and deer at 547,000. Hunters were not required to submit heads of elk in 1998.

Chronic Wasting Disease Information and Regulations

Middle park free of chronic wasting disease DoW press release date: 01/19/1999 "...Sportsmen who hunted in 18 units were required to submit the heads of their harvested deer to the Division during the 1998 big game hunting seasons. Colorado State University pathologists examined the brains of the animals for evidence of infection. More than 350 heads from deer killed in management units 18, 28, 37 and 371 (in the Middle Park area) were submitted and all tested negative for chronic wasting disease. Miller said he is satisfied with the test results of Middle Park, and added that hunters in the Middle Park area will not be required to submit deer heads in 1999.

In addition to the Larimer County units where chronic wasting disease is known to be endemic, sampling was also conducted in the San Luis Valley, Gunnison and an area immediately northeast of Denver to make sure the disease had not spread to those areas. "We didn't expect to find chronic wasting disease in these areas, but we were sampling just to make sure," Miller said. "The results were as expected, with no evidence of the disease."

The incidence of chronic wasting disease in Larimer County remains at about 5 percent on average. In the units east of Larimer County, about 1 to 3 percent of deer on the Platte River drainage tested positive for the disease.

"Base on results over the last several years the incidence of chronic wasting disease in northeastern Colorado is not increasing," Miller said. The Division will continue to monitor chronic wasting disease. For the 1999 hunting seasons, sportsmen in 14 game management units will be required to submit deer heads to the Division for testing. Some units in northeastern Colorado will continue to be sampled. In addition, the Division will test in North Park and may conduct voluntary sampling other West Slope areas.

Units where deer head submission will be required are: 6, 7, 8, 9, 16, 17, 19, 20, 29, 87, 94, 161, 171 and 191. Heads of elk will not be required for submission because less than one percent of 1,000 animals [so about 10 elk -- these may be pooled at game processing facilities affecting everyone's meat -- webmaster] tested in Larimer County during 1996-98 showed any evidence of the disease. Researchers will test elk again in a few years to monitor any changes or possible spread of the disease.

There is no evidence to show that cattle or other domestic livestock can contract the disease, Miller said. [CWD has been passed experimentally to goat -- webmaster] Health department officials added that there is also not evidence that shows humans can contract it.

"There is no indication that chronic wasting disease is a threat to human health," said John Pape, an epidemiologist with the Colorado Department of Public Health and Environment. "But we do recommend that sportsmen who hunt in the area take some common-sense precautions."

Hunters should not take or consume any animal that appears sick, regardless of the cause. Other simple precautions when field dressing game include wearing rubber gloves, minimizing handling of brain and spinal tissues, and washing hands afterwards. Hunters should also avoid consuming brain, spinal cord, eyes, spleen and lymph nodes of animals.

The Division has sought the recommendations from public health officials because chronic wasting disease is one of several diseases collectively called transmissible spongiform encephalopathies. This group of maladies also includes scrapie, a disease of domestic sheep and goats, and bovine spongiform encephalopathy (BSE) that affects some European cattle. British researchers have linked BSE with a new variant of Creutzfeldt-Jakob disease, an extremely rare, but fatal, disease in humans...."

Highlights of Colorado's CWD brochure

dated 17 Nov 97 [received in response to 1 Feb 99 request]: -- "The pathogen that causes this disease has not been identified... Neither the agent causing chronic wasting disease nor its mode of transmission have been identified." The words prion and CJD are nowhere mentioned. -- Scrapie and BSE are discussed as "similar in some respects"; successful experimental transmission to goat is not mentioned though "according to experts, there's no evidence that chronic wasting disease can be transferred naturally to domestic livestock."

-- Range: northern Front Range from Wyoming border south to Lyons and east to Ft. Morgan. Most cases from Estes Park or foothills between Ft. Collins and Loveland.

-- Two cases documented along South Platte River just SE of Larimer County. [Jan 1999 press release gives this as 1-3% of deer in this drainage]

--CWD has been documented in 11 game management units [GMU]; 85% of documented cases are from units 19 and 20.

-- A map showing affected hunting units as of November 1997 is provided. Units 7, 8, 9, 19, 20, 29, 93, 94, 95, 96, and 191 are documented as affected. Units 87, 91, 92, and 954 have mandatory carcass head checks.

-- Lack of enforcement by DoW of feeding stations regs: "Artificial feeding of deer and elk may comound the problem -- in recent years the disease has been most prevalent in areas in the Estes Valley where residents put out feeders to attract deer and elk. Although that practice has been specifically prohibited by regulations approved by the Colorado Wildlife Commission in 1992, many well-meaning individuals coninue to ignore the law and may be exacerbating this problem."

-- Hunter safety: " There is no evidence that chronic wasting disease affects humans, but the Divison of Wildlife advises hunters to take simple precautions when handling the carcass of any deer or elk harvested in the units where CWD occurs Wear rubber gloves when filed dressing carcasses, minimize handling of brain and spinal column and wash hands afterwards. Hunters shoud bone out carcasses or at least avoid consuming brain, spinal cord, eyes, spleen and lymph nodes of harvested animals."



OLD HISTORY COLORADO CWD ALSO SEE;


In September, CWD was found on sev­eral Colorado game farms, which were all subsequently quarantined. The Elk Echo farm alone had 29 elk that contracted the disease and died. The entire herd was slaughtered, and officials then traced elk that were shipped elsewhere. They found 11 more cases at other game farms.

With the exception of one elk in Kansas, Elk Echo elk transported to other states all tested negative.

In April 2002, CWD was found west of the Continental Divide. Reports allege the owner of a game farm near Craig, Colo., erected a fence and trapped wild animals inside. Because laws do not permit farm-raised deer and elk to mix with wild ani­mals, state officials responded and killed 280 wild deer and 30 elk inside the pen. As of this writing, two of 164 tests indi­cated CWD infections.

It is not known how the farm's animals contracted CWD. Owner Wes Adams said he believes the deer were infected before the fence was erected. In a Denver Post article, Adams was quoted as saying he complied with all CWD regulations and that he is the victim, not the cause of the problem. Nevertheless, all 100 elk on his farm will be killed and tested. The farm is 130 miles west of where CWD was found in the wild.

On April 3, Colorado officials began sampling 329 animals within five miles of the farm. On April 9, they reported two deer outside the game farm's fence tested positive. Another deer tested positive a week later, prompting officials to increase their sample quotas.

In Summer 2002, Colorado officials hoped to test at least 300 more deer from areas farther from the CWD epicenter. If no cases are found in fringe areas, it's likely CWD originated in or immediately near the farm. In that case, the state would likely eradicate the farm's animals and nearby wild herds in attempts to slow the disease's spread.

Colorado officials also found CWD near Lyons in Boulder County, where 16 of 77 mule deer from the Rabbit Mountain area tested positive. This 21 percent positive rate is one of the highest ever found in the wild. The discovery caused Boulder County commissioners to approve massive cull hunts aimed at slow­ing a southerly movement of CWD.

The outbreak near Craig also triggered a reaction from Governor Bill Owens, who formed a CWD task force with a charge to review and oversee proactive CWD action in Colorado.

It was also announced that 24 game farmers living near the CWD endemic area agreed to sell their herds to the Department of Agriculture. The USDA planned to slaughter all of the animals and dispose of the carcasses.

END

From: TSS

Subject: Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans (TWO SUSPECT CASES) 

Date: March 13, 2007 at 8:15 am PST

Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans

Lessons From 2 Highly Suspicious but Negative Cases

C. Alan Anderson, MD; Patrick Bosque, MD; Christopher M. Filley, MD; David B. Arciniegas, MD; B. K. Kleinschmidt-DeMasters, MD; W. John Pape, BS; Kenneth L. Tyler, MD 

Arch Neurol. 2007;64:439-441.

Objective To describe 2 patients with rapidly progressive dementia and risk factors for exposure to chronic wasting disease (CWD) in whom extensive testing negated the possible transmission of CWD.

Design/Methods We describe the evaluation of 2 young adults with initial exposure histories and clinical presentations that suggested the possibility of CWD transmission to humans.

Patients A 52-year-old woman with possible laboratory exposure to CWD and a 25-year-old man who had consumed meat from a CWD endemic area.

Interventions Clinical evaluation, neuropathological examination, and genetic testing.

Results Neuropathological and genetic assessment in the 2 patients proved the diagnoses of early-onset Alzheimer disease and a rare genetic prion disease.

Conclusion No convincing cases of CWD transmission to humans have been detected in our surveillance program. 

Author Affiliations: Departments of Neurology (Drs Anderson, Bosque, Filley, Arciniegas, Kleinschmidt-DeMasters, and Tyler), Psychiatry (Drs Anderson, Filley, and Arciniegas), Pathology (Dr Kleinschmidt-DeMasters), Medicine (Dr Tyler), Microbiology (Dr Tyler), and Immunology (Dr Tyler); University of Colorado School of Medicine, Denver; Denver Veterans Affairs Medical Center, Denver (Drs Anderson, Filley, Arciniegas, and Tyler); Denver Health Medical Center, Denver (Dr Bosque); and Colorado Department of Public Health and Environment, Denver (Mr Pape).

http://archneur.ama-assn.org/cgi/content/abstract/64/3/439?ct

> Results Neuropathological and genetic assessment in the 2 patients proved the

> diagnoses of early-onset Alzheimer disease and a rare genetic prion disease

very interesting, and something to ponder here for sure ;

AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

snip...



and i think this would apply to CWD to humans as well.


> rare genetic prion disease

would be interesting to know the exact genetic TSE they are speaking of. GSS, FFI, Familial/Genetic CJD, and or the sporadic FFI that is not genetic, and don't ask me why ??? does not make sense to me either. it's either genetic or not. like i have said many times, the diagnostic criteria differentiating the different human and animal TSE is missing something. but if you have a strain of genetic/familial TSE i.e. FFI, and then you classify a sub-type of that strain that use to be gentic to sporadic, then you have either gone back to sCJD, or the complete damn diagnostic criteria is wrong. you just have well named the damn thing ;

Parchi-Capellari-Chin-Schwarz-Schecter-Butts-Hudkins-Burns-Powers-Gambetti-DISEASE. ...TSS


In Reply to: Re: Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans (TWO SUSPECT CASES) posted by TSS on March 13, 2007 at 8:28 am:

FURTHER into this case study, Colorado Surveillance Program for Chronic Wasting Disease Transmission to Humans (TWO SUSPECT CASES) a look at case 1 and case 2 ;

CASE 1

A 52-year-old right-handed woman presented with a 1-year history of progressive memory loss, language impairment, visuospatial disturbance, and myoclonus. She related that she had been a histology technician in a laboratory that processed tissue specimens from deer and elk with CWD and had handled specimens without wearing gloves. Both she and her family expressed significant concerns about the possibility of transdermal transmission of CWD. Her family history was negative for dementia and other neurologic disorders. Brain magnetic resonance imaging showed mild diffuse volume loss, and electroencephalography demonstrated mild diffuse slowing. Other laboratory studies were unremarkable. Cerebrospinal fluid findings were unremarkable except for a weakly immunostaining 14-3-3 protein band, an indeterminate finding for the diagnosis of prion disease. Genetic testing of the prion protein gene was normal, revealing methionine homozygosity at codon 129. Brain biopsy results were negative for the presence of proteaseresistant prion protein but showed definite Alzheimer disease with numerous neuritic plaques and tau-positive neurofibrillary tangles (Figure). Further analysis of brain tissue at the National Prion Disease Pathology Surveillance Center was negative for prion disease by Western blot analysis. Subsequent investigation by the state department of health revealed the patient had worked in an area of the laboratory that conducted necropsies on domestic animals and had never been assigned to the CWD testing laboratory. The Colorado Department of Public Health and Environment could not confirm that the technician had ever worked with deer and elk tissues.

CASE 2

This 25-year-old right-handed man had a 4-month history of progressive gait disturbance, myoclonus, hallucinations, slowed cognition, impaired attention, and memory loss. He had hunted deer and elk in a CWD endemic area of southern Wyoming and cooked and ate the field-dressed meat. His family history was significant in that his mother had died of a dementing disease at age 40 years, although there was neither a clinical diagnosis nor an autopsy. Brain magnetic resonance imaging findings were unremarkable, and electroencephalography demonstrated 1-Hz high-amplitude periodic sharp wave complexes. Other laboratory studies had negative results. Testing for the 14-3-3 protein had positive results, but the cerebrospinal fluid was otherwise unremarkable. The diagnosis of Gerstmann-Stra¨ussler-Scheinker syndrome, a familial prion disease, was confirmed with a detailed autopsy examination and referral of the brain to the National Prion Disease Pathology Surveillance Center. Autopsy brain tissue showed the presence of proteaseresistant prion protein by Western blot analysis. Genetic evaluation revealed the P102L mutation in the prion protein gene with methionine/valine heterozygosity at codon 129.

snip...end 

I can't understand how they can keep claiming 'low, or no occupational transmission of CJD' ??? when there have been many cases that should have raised awareness, and in some cases they did, only to be swept under the rug as the infamous sporadic CJD, or some other TSE other than the nvCJD of the ukbsenvcjd only theory. it's a blown theory no one will accept too. lets look at a few occupational cases. ...TSS

now, some things to ponder ;

Questions:

1. Do neuritic plaques and tau-positive neurofibrillary tangles indicate definite AD? Aren't these also found in GSS? What about concurrent AD and TSE?

2. Are the NPDPSC results conclusive? Do WB results depend on the part of the brain sampled?

3. Doesn't it seem unlikely the woman would flat-out lie about working with CWD tissues? (I'm working on this locally.)

4. What about cross-contamination? The lab gets large numbers of scrapie-infected sheep and CWD-infected deer and elk. I assume the necropsy area is contaminated with TSEs. ...end...tss

UPDATE* NOVEMBER 16, 2014 vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ??? Friday, January 10, 2014 

Greetings again Friends, Neighbors, and Colleagues, 

I would kindly like to follow up on ‘vpspr, sgss, sffi, TSE, an iatrogenic by-product of gss, ffi, familial type prion disease, what it ???’ ran across an old paper from 1984, that some might find interest in, and I will update the link with this old science paper from 1984, a 2010 paper from Japan, and some information on scrapie transmission. The paper from Japan first, then the 1984 paper, and then the scrapie transmission studies. 

***The occurrence of contact cases raises the possibility that transmission in families may be effected by an unusually virulent strain of the agent. 





SCRAPIE AND CWD IN CERVID, WHAT IF?


White-tailed Deer are Susceptible to Scrapie by Natural Route of Infection

Jodi D. Smith, Justin J. Greenlee, and Robert A. Kunkle; Virus and Prion Research Unit, National Animal Disease Center, USDA-ARS
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by potential natural routes of inoculation. In-depth analysis of tissues will be done to determine similarities between scrapie in deer after intracranial and oral/intranasal inoculation and chronic wasting disease resulting from similar routes of inoculation.
see full text ;
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
White-tailed deer are susceptible to the agent of sheep scrapie by intracerebral inoculation
snip...
It is unlikely that CWD will be eradicated from free-ranging cervids, and the disease is likely to continue to spread geographically [10]. However, the potential that white-tailed deer may be susceptible to sheep scrapie by a natural route presents an additional confounding factor to halting the spread of CWD. This leads to the additional speculations that
1) infected deer could serve as a reservoir to infect sheep with scrapie offering challenges to scrapie eradication efforts and
2) CWD spread need not remain geographically confined to current endemic areas, but could occur anywhere that sheep with scrapie and susceptible cervids cohabitate.
This work demonstrates for the first time that white-tailed deer are susceptible to sheep scrapie by intracerebral inoculation with a high attack rate and that the disease that results has similarities to CWD. These experiments will be repeated with a more natural route of inoculation to determine the likelihood of the potential transmission of sheep scrapie to white-tailed deer. If scrapie were to occur in white-tailed deer, results of this study indicate that it would be detected as a TSE, but may be difficult to differentiate from CWD without in-depth biochemical analysis.
2012
PO-039: A comparison of scrapie and chronic wasting disease in white-tailed deer
Justin Greenlee, Jodi Smith, Eric Nicholson US Dept. Agriculture; Agricultural Research Service, National Animal Disease Center; Ames, IA USA
snip...
The results of this study suggest that there are many similarities in the manifestation of CWD and scrapie in WTD after IC inoculation including early and widespread presence of PrPSc in lymphoid tissues, clinical signs of depression and weight loss progressing to wasting, and an incubation time of 21-23 months. Moreover, western blots (WB) done on brain material from the obex region have a molecular profile similar to CWD and distinct from tissues of the cerebrum or the scrapie inoculum. However, results of microscopic and IHC examination indicate that there are differences between the lesions expected in CWD and those that occur in deer with scrapie: amyloid plaques were not noted in any sections of brain examined from these deer and the pattern of immunoreactivity by IHC was diffuse rather than plaque-like.
*** After a natural route of exposure, 100% of WTD were susceptible to scrapie.
Deer developed clinical signs of wasting and mental depression and were necropsied from 28 to 33 months PI. Tissues from these deer were positive for PrPSc by IHC and WB. Similar to IC inoculated deer, samples from these deer exhibited two different molecular profiles: samples from obex resembled CWD whereas those from cerebrum were similar to the original scrapie inoculum. On further examination by WB using a panel of antibodies, the tissues from deer with scrapie exhibit properties differing from tissues either from sheep with scrapie or WTD with CWD. Samples from WTD with CWD or sheep with scrapie are strongly immunoreactive when probed with mAb P4, however, samples from WTD with scrapie are only weakly immunoreactive. In contrast, when probed with mAb’s 6H4 or SAF 84, samples from sheep with scrapie and WTD with CWD are weakly immunoreactive and samples from WTD with scrapie are strongly positive. This work demonstrates that WTD are highly susceptible to sheep scrapie, but on first passage, scrapie in WTD is differentiable from CWD.
2011
*** After a natural route of exposure, 100% of white-tailed deer were susceptible to scrapie.
Sunday, October 25, 2015
USAHA Detailed Events Schedule – 119th USAHA Annual Meeting CAPTIVE LIVESTOCK CWD SCRAPIE TSE PRION

snip...see more here ;

TUESDAY, MARCH 28, 2017 

*** Passage of scrapie to deer results in a new phenotype upon return passage to sheep ***



From: TSS

Subject: Recent death may be Creutzfeldt-Jakob Disease Fort Collins Colorado 

Date: January 28, 2006 at 7:53 am PST

Fort Collins Coloradoan Article published Jan 27, 2006

Recent death may be Creutzfeldt-Jakob Biopsy will tell if brain-wasting disease is to blame

By KEVIN DARST KevinDarst@coloradoan.com

The brain of a Fort Collins woman who died earlier this week will be tested for Creutzfeldt-Jakob disease, a rare brain-wasting disease, a state official confirmed.

Nancy Banks, 69, died Monday, just two months after suffering stroke-like symptoms that her neurologist later determined to be CJD, according to her obituary.

Colorado has had 39 cases of CJD since the state began monitoring the disease in 1998 - an average of 4.9 cases a year, said John Pape, the state epidemiologist. Banks is the second person to be tested this year for the disease.

"We've had a couple listed as CJD on the death certificate but turn out not to be (CJD) at the autopsy," Pape said.

An autopsy or brain biopsy is the only way to confirm a CJD diagnosis, though not all the cases counted by the state had autopsies, Pape said. Tests also can identify the type of CJD: sporadic, hereditary, acquired or variant.

There is no treatment or cure for the disease, and about 90 percent of people with the disease die within a year, according to the National Institute of Health's National Institute of Neurological Disorders and Stroke. CJD causes memory failures, behavioral changes, coordination and vision problems, according to the institute. It can also cause mental deterioration, involuntary movement, blindness, weakness and coma as it advances.

The average person stricken with classic CJD is 68 years old and lives four to five months after symptoms set in, according to the U.S. Centers for Disease Control and Prevention.

CJD belongs to a group of diseases called transmissible spongiform encephalopathies that includes chronic wasting disease in deer and elk, scrapie in sheep and bovine spongiform encephalopathy, or mad cow disease, in cattle. The diseases are caused by abnormal proteins called prions.

About 93 percent of the 1,133 CJD cases in the U.S. since 1997 have been sporadic or hereditary, according to a Coloradoan analysis of CJD surveillance by the National Prion Disease Pathology Surveillance Center at Case Western Reserve University in Cleveland.

"About 90 percent of CJD cases are sporadic," said Dr. Patrick Bosque, a neurologist and prion researcher at Denver Health Medical Center. "The one concern in Colorado is, could it be related to deer?"

Just one person in the U.S. has died from vCJD, and that person likely acquired the disease in the United Kingdom, according to the surveillance center. Colorado never has had a verified vCJD case, Pape said.

Nearly 160 people worldwide, most from the United Kingdom, are known to have contracted the variant type of the disease after they ate beef from cattle with mad cow disease.

Banks, born in Denver, spent nearly two decades as head of the Library and Media Center of Riffenburgh Elementary School before moving to the LINC Library, a summer reading program of the Fort Collins Library and the Poudre School District, according to the obituary. She also started a library at First Christian Church.

Samples collected from Banks will be sent to the National Prion Disease Pathology Surveillance Center. It could be several months before results are available, Pape said.

Pape declined to say who was collecting the samples from Banks. He said it's difficult to find coroners or physicians willing to do autopsies on potential CJD victims because there's a small risk of catching the disease if infected material comes in contact with an open cut or orifice.

"There's some concern with autopsies and contamination and exposure," Pape said. "A lot of coroners and hospitals absolutely will not do them."

Though the disease is rare, Pape said he believes awareness is "heightened" among the neurologists he's talked to in the state.

"There are some hallmarks that can clue in a neurologist," Pape said.

When contacted by the Coloradoan, Banks' daughter, Afton Rorvik, said it was too difficult at this time to talk about her mother's illness and death. 

http://www.coloradoan.com/apps/pbcs.dll/articleAID=/20060127/NEWS01/601270315/1002 

Nancy Banks Born in Denver, CO Departed on Jan. 23, 2006 and resided in Fort Collins, CO. 

Memorial Service: Saturday Jan. 28, 2006 Cemetery: Private Please click on the links above for locations, times, maps, and directions. 

Knitting. Nancy Banks knitted in the dark, at meetings, on the telephone, during movies. As she drove down the highway in her silver Honda civic, her thumbs and forefingers sometimes twitched up and down, as if she were impatient to get back to whatever important project she was creating. Yarn and cloth bags containing various knitting projects could be found all over her house.

Born in 1936, in post-depression Denver, Colorado, Nancy’s mother taught her the rudiments of knitting at the age of five. Like most other things, Nancy approached knitting with energy, confidence, and a totally unique, self-taught approach. Sweaters for children, decorated blankets for married couples and grandchildren, baby booties and hats, crazy striped socks, scarves, and Christmas ornaments poured off her needles in a constant stream.

Nancy also understood and loved the written word. At her high school, the Kent school for girls, she edited the yearbook, and went on to Smith College, where she majored in German literature (after a brief flirtation with physics!) Her love of books led her to a Masters of Library Science from the University of Denver in 1973, and she headed the Library and Media Center of Riffenburgh Elementary School shortly after graduating.

In addition to repairing audio-visual equipment, and keeping the large collection of books, materials and computer equipment in order, Nancy understood her role as a caregiver, and a mentor. She loved making the library a safe, loving place for children. She brought her huge stuffed Gorilla named “George” to her story hour for them to hold, held programming classes, and helped a group of interested young students start a “Tolkien” group, exploring the world and mythologies of the author of “The Lord of the Rings.”

After retiring from Riffenburgh almost 10 years ago, Nancy went to work on the LINC program, a summer reading program that meshed resources and personnel from both the Fort Collins Public Library and the Poudre R1 School District. Her years in the schools helped her create a program that enabled families to come to events hosted at their local school library over the summer, and encouraged them and their children to read. The LINC programs, offered by members of the Fort Collins community, often followed her own broad interests: opera, dog-sledding, physics, and of course knitting.

During the time she could spare from the LINC program, Nancy traveled widely. Her favorite international places included Germany (where she had spent a year studying in 1958), England, Ireland and Wales (where she vividly remembered hearing of the September 11 tragedy.) She also regularly visited her close friends and family all over the United States, especially prioritizing spending time with her six grandchildren. Equally at home in the car or the airport, she only became anxious when airport security once confiscated her knitting needles, apparently deciding that this tall, striking woman in her 60’s needed disarming.

Nancy’s faith was strong, and she worked hard to help others. She established a library at First Christian Church, and a cassette tape ministry that made sermons available to those who weren’t physically able to attend services. She also loved singing in the choir, occasionally playing violin in the church orchestra. After moving her church home to First Presbyterian, she kept singing, adding her strong alto voice and determined energy to the choir. She also began visiting people on behalf of the church, in hospitals and in their homes. Her bible study, and her work there as a deacon were exceptionally important to her, and her strength and kindness helped her make lasting friendships wherever she went.

In late November of 2005, Nancy was admitted to Albany Medical Center, having shown stroke-like symptoms while visiting one of her sons for Thanksgiving. After some analysis, the neurologists determined that she had Cruetzfeldt-Jakob’s disease, an extremely rare neurodegenerative disease which is fatal within months of the onset of symptoms.

In spite of her diagnosis, Nancy continued energetically adapting to the burdens of the disease, remaining open and in good spirits through the end. In the three months of her illness, she was constantly surrounded by her family and her extensive community of friends. As we all understand the depth of her love and involvement with so many people, it’s clear that her largest knitting project is now complete – a beautiful tapestry of people connected with one another. She must be very pleased.

Nancy is preceded in death by her parents, Thompson George Marsh and Susan Raymond Marsh, and by her ex-husband Loy Banks.

She is survived by her three sisters, Alice Abbot, Lucy Marsh, and Mary Zulack, her three children, William Banks, Afton Rorvik, and Joseph Banks, and her 6 grandchildren, Ian Banks, Karl Rorvik, Stephen Banks, Robert Banks, Annalisa Rorvik, and Mark Banks. 

http://obit.allnutt.com/obit_display.cgi?id=282112&listing=Current 

GUESTBOOK My heartfelt sympathy to the family of Nancy. Although I did not know her I especially feel your loss today because my 48 year old brother also passed from CJD 11 years ago. That was the 1st time I had heard of the disease. I too share a love of knitting. My prayers are with you all.

Jana Skradski Jan 27, 2006 Fort Collins, CO

Fort Collins, CO

City Population 2000: 118,652

Metro area: Fort Collins-Loveland 

Colorado — Population: 4,301,261 ; 24th, 12/00 According to http://www.50states.com/colorado.htm

question;

did she consume venison?

did she have surgery, where others that have consumed venison, that might have been exposed to CWD had surgery?

did she donate blood?

how many have been exposed via the surgical/medical arena by CWD in this area?

PAGE 22 

IN CONFIDENCE 

http://www.bseinquiry.gov.uk/files/mb/m11b/tab01.pdf 

Subject: Prions in Skeletal Muscles of Deer with Chronic Wasting Disease [SCIENCE FULL TEXT] Date: January 26, 2006 at 12:23 pm PST

Prions in Skeletal Muscles of Deer with Chronic Wasting Disease 

Rachel C. Angers,1* Shawn R. Browning,1*† Tanya S. Seward,2 Christina J. Sigurdson,4‡ Michael W. Miller,5 Edward A. Hoover,4 Glenn C. Telling1,2,3§

1Department of Microbiology, Immunology and Molecular Genetics, 2Sanders Brown Center on Aging, 3Department of Neurology, University of Kentucky, Lexington, KY 40536, USA. 4Department of Microbiology, Immunology and Pathology, Colorado State University, Fort Collins, CO 80523, USA. 5Colorado Division of Wildlife, Wildlife Research Center, Fort Collins, CO 80526, USA.

*These authors contributed equally to this work.

†Present address: Department of Infectology, Scripps Research Institute, 5353 Parkside Drive, RF-2, Jupiter, Florida, 33458, USA.

‡Present address: Institute of Neuropathology, University of Zurich, Schmelzbergstrasse 12, 8091 Zurich, Switzerland.

§To whom correspondence should be addressed: E-mail: gtell2@uky.edu

Prions are transmissible proteinaceous agents of mammals that cause fatal neurodegenerative diseases of the central nervous system (CNS). The presence of infectivity in skeletal muscle of experimentally infected mice raised the possibility that dietary exposure to prions might occur through meat consumption (1). Chronic wasting disease (CWD), an enigmatic and contagious prion disease of North American cervids, is of particular concern. The emergence of CWD in an increasingly wide geographic area and the interspecies transmission of bovine spongiform encephalopathy (BSE) to humans as variant Creutzfeldt Jakob disease (vCJD) have raised concerns about zoonotic transmission of CWD.

To test whether skeletal muscle of diseased cervids contained prion infectivity, Tg(CerPrP)1536 mice (2) expressing cervid prion protein (CerPrP), were inoculated intracerebrally with extracts prepared from the semitendinosus/semimembranosus muscle group of CWD-affected mule deer or from CWD-negative deer. The availability of CNS materials also afforded direct comparisons of prion infectivity in skeletal muscle and brain. All skeletal muscle extracts from CWD-affected deer induced progressive neurological dysfunction in Tg(CerPrP)1536 mice with mean incubation times ranging between 360 and ~490 d, whereas the incubation times of prions from the CNS ranged from ~230 to 280 d (Table 1). For each inoculation group, the diagnosis of prion disease was confirmed by the presence of PrPSc in the brains of multiple infected Tg(CerPrP)1536 mice (see supporting online material for examples). In contrast, skeletal muscle and brain material from CWD-negative deer failed to induce disease in Tg(CerPrP)1536 mice (Table 1) and PrPSc was not detected in the brains of sacrificed asymptomatic mice as late as 523 d after inoculation (supporting online material).

Our results show that skeletal muscle as well as CNS tissue of deer with CWD contains infectious prions. Similar analyses of skeletal muscle BSE-affected cattle did not reveal high levels of prion infectivity (3). It will be important to assess the cellular location of PrPSc in muscle. Notably, while PrPSc has been detected in muscles of scrapie-affected sheep (4), previous studies failed to detect PrPSc by immunohistochemical analysis of skeletal muscle from deer with natural or experimental CWD (5, 6). Since the time of disease onset is inversely proportional to prion dose (7), the longer incubation times of prions from skeletal muscle extracts compared to matched brain samples indicated that prion titers were lower in muscle than in CNS where infectivity titers are known to reach high levels. Although possible effects of CWD strains or strain mixtures on these incubation times cannot be excluded, the variable 360 to ~490 d incubation times suggested a range of prion titers in skeletal muscles of CWD-affected deer. Muscle prion titers at the high end of the range produced the fastest incubation times that were ~30% longer than the incubation times of prions from the CNS of the same animal. Since all mice in each inoculation group developed disease, prion titers in muscle samples producing the longest incubation times were higher than the end point of the bioassay, defined as the infectious dose at which half the inoculated mice develop disease. Studies are in progress to accurately assess prion titers.

While the risk of exposure to CWD infectivity following consumption of prions in muscle is mitigated by relatively inefficient prion transmission via the oral route (8), these 

results show that semitendinosus/semimembranosus muscle, which is likely to be consumed by humans, is a significant source of prion infectivity. Humans consuming or handling meat from CWD-infected deer are therefore at risk to prion exposure.

References and Notes

1. P. J. Bosque et al., Proc. Natl. Acad. Sci. U.S.A. 99, 3812 (2002).

2. S. R. Browning et al., J. Virol. 78, 13345 (2004).

3. A. Buschmann, M. H. Groschup, J. Infect. Dis. 192, 934 (2005).

4. O. Andreoletti et al., Nat. Med. 10, 591 (2004).

5. T. R. Spraker et al., Vet. Pathol. 39, 110 (2002).

6. A. N. Hamir, J. M. Miller, R. C. Cutlip, Vet. Pathol. 41, 78 (2004).

7. S. B. Prusiner et al., Biochemistry 21, 4883 (1980).

8. M. Prinz et al., Am. J. Pathol. 162, 1103 (2003).

9. This work was supported by grants from the U.S. Public Health Service 2RO1 NS040334-04 from the National Institute of Neurological Disorders and Stroke and N01-AI-25491 from the National Institute of Allergy and Infectious Diseases.

Supporting Online Material

www.sciencemag.org/

HUMAN TSE USA 2005 

Animal Prion Diseases Relevant to Humans (unknown types?) Thu Oct 27, 2005 12:05 71.248.128.109 

About Human Prion Diseases / Animal Prion Diseases Relevant to Humans

Bovine Spongiform Encephalopathy (BSE) is a prion disease of cattle. Since 1986, when BSE was recognized, over 180,000 cattle in the UK have developed the disease, and approximately one to three million are likely to have been infected with the BSE agent, most of which were slaughtered for human consumption before developing signs of the disease. The origin of the first case of BSE is unknown, but the epidemic was caused by the recycling of processed waste parts of cattle, some of which were infected with the BSE agent and given to other cattle in feed. Control measures have resulted in the consistent decline of the epidemic in the UK since 1992. Infected cattle and feed exported from the UK have resulted in smaller epidemics in other European countries, where control measures were applied later.

Compelling evidence indicates that BSE can be transmitted to humans through the consumption of prion contaminated meat. BSE-infected individuals eventually develop vCJD with an incubation time believed to be on average 10 years. As of November 2004, three cases of BSE have been reported in North America. One had been imported to Canada from the UK, one was grown in Canada, and one discovered in the USA but of Canadian origin. There has been only one case of vCJD reported in the USA, but the patient most likely acquired the disease in the United Kingdom. If current control measures intended to protect public and animal health are well enforced, the cattle epidemic should be largely under control and any remaining risk to humans through beef consumption should be very small. (For more details see Smith et al. British Medical Bulletin, 66: 185. 2003.)

Chronic Wasting Disease (CWD) is a prion disease of elk and deer, both free range and in captivity. CWD is endemic in areas of Colorado, Wyoming, and Nebraska, but new foci of this disease have been detected in Nebraska, South Dakota, New Mexico, Wisconsin, Mississippi Kansas, Oklahoma, Minnesota, Montana, and Canada. Since there are an estimated 22 million elk and deer in the USA and a large number of hunters who consume elk and deer meat, there is the possibility that CWD can be transmitted from elk and deer to humans. As of November 2004, the NPDPSC has examined 26 hunters with a suspected prion disease. However, all of them appeared to have either typical sporadic or familial forms of the disease. The NPDPSC coordinates with the Centers for Disease Control and state health departments to monitor cases from CWD-endemic areas. Furthermore, it is doing experimental research on CWD transmissibility using animal models. (For details see Sigurdson et al. British Medical Bulletin. 66: 199. 2003 and Belay et al. Emerging Infectious Diseases. 10(6): 977. 2004.) 

http://www.cjdsurveillance.com/abouthpd-animal.html 

SEE STEADY INCREASE IN SPORADIC CJD IN THE USA FROM 1997 TO 2004. SPORADIC CJD CASES TRIPLED, and that is with a human TSE surveillance system that is terrible flawed. in 1997 cases of the _reported_ cases of cjd were at 54, to 163 _reported_ cases in 2004. see stats here;

p.s. please note the 47 PENDING CASES to Sept. 2005

p.s. please note the 2005 Prion D. total 120(8) 8=includes 51 type pending, 1 TYPE UNKNOWN ???

p.s. please note sporadic CJD 2002(1) 1=3 TYPE UNKNOWN???

p.s. please note 2004 prion disease (6) 6=7 TYPE UNKNOWN??? 

http://www.cjdsurveillance.com/resources-casereport.html 

CWD TO HUMANS = sCJD ??? 

AS implied in the Inset 25 we must not _ASSUME_ that transmission of BSE to other species will invariably present pathology typical of a scrapie-like disease.

snip...

http://www.bseinquiry.gov.uk/files/yb/1991/01/04004001.pdf 

ATYPICAL TSEs in USA CATTLE AND SHEEP ? 

http://www.bseinquiry.gov.uk/files/sc/seac17/tab03.pdf 

WHAT WILL CWDTSE IN HUMAN LOOK LIKE??? 

TSS 




TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT First evidence of intracranial and peroral transmission of Chronic Wasting Disease (CWD) into Cynomolgus macaques: a work in progress


 BSE INQUIRY

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). *** 

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). *** 

*** The association between venison eating and risk of CJD shows similar pattern, with regular venison eating associated with a 9 FOLD INCREASE IN RISK OF CJD (p = 0.04). *** 

There is some evidence that risk of CJD INCREASES WITH INCREASING FREQUENCY OF LAMB EATING (p = 0.02). The evidence for such an association between beef eating and CJD is weaker (p = 0.14). When only controls for whom a relative was interviewed are included, this evidence becomes a little STRONGER (p = 0.08). 

snip... 

It was found that when veal was included in the model with another exposure, the association between veal and CJD remained statistically significant (p = < 0.05 for all exposures), while the other exposures ceased to be statistically significant (p = > 0.05). 

snip... 

In conclusion, an analysis of dietary histories revealed statistical associations between various meats/animal products and INCREASED RISK OF CJD. When some account was taken of possible confounding, the association between VEAL EATING AND RISK OF CJD EMERGED AS THE STRONGEST OF THESE ASSOCIATIONS STATISTICALLY. ... 

snip... 

In the study in the USA, a range of foodstuffs were associated with an increased risk of CJD, including liver consumption which was associated with an apparent SIX-FOLD INCREASE IN THE RISK OF CJD. By comparing the data from 3 studies in relation to this particular dietary factor, the risk of liver consumption became non-significant with an odds ratio of 1.2 (PERSONAL COMMUNICATION, PROFESSOR A. HOFMAN. ERASMUS UNIVERSITY, ROTTERDAM). (???...TSS) 

snip...see full report ; 


NEW URL LINK; 


you can see more evidence here ;


TUESDAY, JULY 04, 2017

*** PRION 2017 CONFERENCE ABSTRACTS ON CHRONIC WASTING DISEASE CWD TSE PRION ***


TUESDAY, JUNE 13, 2017

PRION 2017 CONFERENCE ABSTRACT Chronic Wasting Disease in European moose is associated with PrPSc features different from North American CWD



Wednesday, May 24, 2017 

PRION2017 CONFERENCE VIDEO UPDATE 23 – 26 May 2017 Edinburgh UPDATE 1



URINE

SUNDAY, JULY 16, 2017

*** Temporal patterns of chronic wasting disease prion excretion in three cervid species ***


*** WDA 2016 NEW YORK *** 

 We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. 

 Student Presentations Session 2 

 The species barriers and public health threat of CWD and BSE prions 

 Ms. Kristen Davenport1, Dr. Davin Henderson1, Dr. Candace Mathiason1, Dr. Edward Hoover1 1Colorado State University 

 Chronic wasting disease (CWD) is spreading rapidly through cervid populations in the USA. Bovine spongiform encephalopathy (BSE, mad cow disease) arose in the 1980s because cattle were fed recycled animal protein. These and other prion diseases are caused by abnormal folding of the normal prion protein (PrP) into a disease causing form (PrPd), which is pathogenic to nervous system cells and can cause subsequent PrP to misfold. CWD spreads among cervids very efficiently, but it has not yet infected humans. On the other hand, BSE was spread only when cattle consumed infected bovine or ovine tissue, but did infect humans and other species. The objective of this research is to understand the role of PrP structure in cross-species infection by CWD and BSE. To study the propensity of each species’ PrP to be induced to misfold by the presence of PrPd from verious species, we have used an in vitro system that permits detection of PrPd in real-time. We measured the conversion efficiency of various combinations of PrPd seeds and PrP substrate combinations. We observed the cross-species behavior of CWD and BSE, in addition to feline-adapted CWD and BSE. We found that CWD adapts to a new host more readily than BSE and that human PrP was unexpectedly prone to misfolding by CWD prions. In addition, we investigated the role of specific regions of the bovine, deer and human PrP protein in resistance to conversion by prions from another species. 

*** We have concluded that the human protein has a region that confers unusual susceptibility to conversion by CWD prions. 

*** CWD is unique among prion diseases in its rapid spread in natural populations. 

*** BSE prions are essentially unaltered upon passage to a new species, while CWD adapts to the new species. 

*** This adaptation has consequences for surveillance of humans exposed to CWD. 

 Wildlife Disease Risk Communication Research Contributes to Wildlife Trust Administration Exploring perceptions about chronic wasting disease risks among wildlife and agriculture professionals and stakeholders 


you can see more evidence here ; 


Transmission of scrapie prions to primate after an extended silent incubation period 

Emmanuel E. Comoy, Jacqueline Mikol, Sophie Luccantoni-Freire, Evelyne Correia, Nathalie Lescoutra-Etchegaray, Valérie Durand, Capucine Dehen, Olivier Andreoletti, Cristina Casalone, Juergen A. Richt, Justin J. Greenlee, Thierry Baron, Sylvie L. Benestad, Paul Brown & Jean-Philippe Deslys

Scientific Reports 5, Article number: 11573 (2015) doi:10.1038/srep11573

Download Citation EpidemiologyNeurological manifestationsPrion diseases Received: 16 February 2015 Accepted: 28 May 2015 Published online: 30 June 2015

Abstract

Classical bovine spongiform encephalopathy (c-BSE) is the only animal prion disease reputed to be zoonotic, causing variant Creutzfeldt-Jakob disease (vCJD) in humans and having guided protective measures for animal and human health against animal prion diseases. Recently, partial transmissions to humanized mice showed that the zoonotic potential of scrapie might be similar to c-BSE. We here report the direct transmission of a natural classical scrapie isolate to cynomolgus macaque, a highly relevant model for human prion diseases, after a 10-year silent incubation period, with features similar to those reported for human cases of sporadic CJD. Scrapie is thus actually transmissible to primates with incubation periods compatible with their life expectancy, although fourfold longer than BSE. Long-term experimental transmission studies are necessary to better assess the zoonotic potential of other prion diseases with high prevalence, notably Chronic Wasting Disease of deer and elk and atypical/Nor98 scrapie. 

snip... 

Discussion We describe the transmission of spongiform encephalopathy in a non-human primate inoculated 10 years earlier with a strain of sheep c-scrapie. Because of this extended incubation period in a facility in which other prion diseases are under study, we are obliged to consider two alternative possibilities that might explain its occurrence. We first considered the possibility of a sporadic origin (like CJD in humans). Such an event is extremely improbable because the inoculated animal was 14 years old when the clinical signs appeared, i.e. about 40% through the expected natural lifetime of this species, compared to a peak age incidence of 60–65 years in human sporadic CJD, or about 80% through their expected lifetimes. Moreover, sporadic disease has never been observed in breeding colonies or primate research laboratories, most notably among hundreds of animals over several decades of study at the National Institutes of Health25, and in nearly twenty older animals continuously housed in our own facility.

The second possibility is a laboratory cross-contamination. Three facts make this possibility equally unlikely. First, handling of specimens in our laboratory is performed with fastidious attention to the avoidance of any such cross-contamination. Second, no laboratory cross-contamination has ever been documented in other primate laboratories, including the NIH, even between infected and uninfected animals housed in the same or adjacent cages with daily intimate contact (P. Brown, personal communication). Third, the cerebral lesion profile is different from all the other prion diseases we have studied in this model19, with a correlation between cerebellar lesions (massive spongiform change of Purkinje cells, intense PrPres staining and reactive gliosis26) and ataxia. The iron deposits present in the globus pallidus are a non specific finding that have been reported previously in neurodegenerative diseases and aging27. Conversely, the thalamic lesion was reminiscent of a metabolic disease due to thiamine deficiency28 but blood thiamine levels were within normal limits (data not shown). The preferential distribution of spongiform change in cortex associated with a limited distribution in the brainstem is reminiscent of the lesion profile in MM2c and VV1 sCJD patients29, but interspecies comparison of lesion profiles should be interpreted with caution. It is of note that the same classical scrapie isolate induced TSE in C57Bl/6 mice with similar incubation periods and lesional profiles as a sample derived from a MM1 sCJD patient30.

We are therefore confident that the illness in this cynomolgus macaque represents a true transmission of a sheep c-scrapie isolate directly to an old-world monkey, which taxonomically resides in the primate subdivision (parvorder of catarrhini) that includes humans. With an homology of its PrP protein with humans of 96.4%31, cynomolgus macaque constitutes a highly relevant model for assessing zoonotic risk of prion diseases. Since our initial aim was to show the absence of transmission of scrapie to macaques in the worst-case scenario, we obtained materials from a flock of naturally-infected sheep, affecting animals with different genotypes32. This c-scrapie isolate exhibited complete transmission in ARQ/ARQ sheep (332 ± 56 days) and Tg338 transgenic mice expressing ovine VRQ/VRQ prion protein (220 ± 5 days) (O. Andreoletti, personal communication). From the standpoint of zoonotic risk, it is important to note that sheep with c-scrapie (including the isolate used in our study) have demonstrable infectivity throughout their lymphoreticular system early in the incubation period of the disease (3 months-old for all the lymphoid organs, and as early as 2 months-old in gut-associated lymph nodes)33. In addition, scrapie infectivity has been identified in blood34, milk35 and skeletal muscle36 from asymptomatic but scrapie infected small ruminants which implies a potential dietary exposure for consumers.

Two earlier studies have reported the occurrence of clinical TSE in cynomolgus macaques after exposures to scrapie isolates. In the first study, the “Compton” scrapie isolate (derived from an English sheep) and serially propagated for 9 passages in goats did not transmit TSE in cynomolgus macaque, rhesus macaque or chimpanzee within 7 years following intracerebral challenge1; conversely, after 8 supplementary passages in conventional mice, this “Compton” isolate induced TSE in a cynomolgus macaque 5 years after intracerebral challenge, but rhesus macaques and chimpanzee remained asymptomatic 8.5 years post-exposure8. However, multiple successive passages that are classically used to select laboratory-adapted prion strains can significantly modify the initial properties of a scrapie isolate, thus questioning the relevance of zoonotic potential for the initial sheep-derived isolate. The same isolate had also induced disease into squirrel monkeys (new-world monkey)9. A second historical observation reported that a cynomolgus macaque developed TSE 6 years post-inoculation with brain homogenate from a scrapie-infected Suffolk ewe (derived from USA), whereas a rhesus macaque and a chimpanzee exposed to the same inoculum remained healthy 9 years post-exposure1. This inoculum also induced TSE in squirrel monkeys after 4 passages in mice. Other scrapie transmission attempts in macaque failed but had more shorter periods of observation in comparison to the current study. Further, it is possible that there are differences in the zoonotic potential of different scrapie strains.

The most striking observation in our study is the extended incubation period of scrapie in the macaque model, which has several implications. Firstly, our observations constitute experimental evidence in favor of the zoonotic potential of c-scrapie, at least for this isolate that has been extensively studied32,33,34,35,36. The cross-species zoonotic ability of this isolate should be confirmed by performing duplicate intracerebral exposures and assessing the transmissibility by the oral route (a successful transmission of prion strains through the intracerebral route may not necessarily indicate the potential for oral transmission37). However, such confirmatory experiments may require more than one decade, which is hardly compatible with current general management and support of scientific projects; thus this study should be rather considered as a case report.

Secondly, transmission of c-BSE to primates occurred within 8 years post exposure for the lowest doses able to transmit the disease (the survival period after inoculation is inversely proportional to the initial amount of infectious inoculum). The occurrence of scrapie 10 years after exposure to a high dose (25 mg) of scrapie-infected sheep brain suggests that the macaque has a higher species barrier for sheep c-scrapie than c-BSE, although it is notable that previous studies based on in vitro conversion of PrP suggested that BSE and scrapie prions would have a similar conversion potential for human PrP38.

Thirdly, prion diseases typically have longer incubation periods after oral exposure than after intracerebral inoculations: since humans can develop Kuru 47 years after oral exposure39, an incubation time of several decades after oral exposure to scrapie would therefore be expected, leading the disease to occur in older adults, i.e. the peak age for cases considered to be sporadic disease, and making a distinction between scrapie-associated and truly sporadic disease extremely difficult to appreciate.

Fourthly, epidemiologic evidence is necessary to confirm the zoonotic potential of an animal disease suggested by experimental studies. A relatively short incubation period and a peculiar epidemiological situation (e.g., all the first vCJD cases occurring in the country with the most important ongoing c-BSE epizootic) led to a high degree of suspicion that c-BSE was the cause of vCJD. Sporadic CJD are considered spontaneous diseases with an almost stable and constant worldwide prevalence (0.5–2 cases per million inhabitants per year), and previous epidemiological studies were unable to draw a link between sCJD and classical scrapie6,7,40,41, even though external causes were hypothesized to explain the occurrence of some sCJD clusters42,43,44. However, extended incubation periods exceeding several decades would impair the predictive values of epidemiological surveillance for prion diseases, already weakened by a limited prevalence of prion diseases and the multiplicity of isolates gathered under the phenotypes of “scrapie” and “sporadic CJD”.

Fifthly, considering this 10 year-long incubation period, together with both laboratory and epidemiological evidence of decade or longer intervals between infection and clinical onset of disease, no premature conclusions should be drawn from negative transmission studies in cynomolgus macaques with less than a decade of observation, as in the aforementioned historical transmission studies of scrapie to primates1,8,9. Our observations and those of others45,46 to date are unable to provide definitive evidence regarding the zoonotic potential of CWD, atypical/Nor98 scrapie or H-type BSE. The extended incubation period of the scrapie-affected macaque in the current study also underscores the limitations of rodent models expressing human PrP for assessing the zoonotic potential of some prion diseases since their lifespan remains limited to approximately two years21,47,48. This point is illustrated by the fact that the recently reported transmission of scrapie to humanized mice was not associated with clinical signs for up to 750 days and occurred in an extreme minority of mice with only a marginal increase in attack rate upon second passage13. The low attack rate in these studies is certainly linked to the limited lifespan of mice compared to the very long periods of observation necessary to demonstrate the development of scrapie. Alternatively, one could estimate that a successful second passage is the result of strain adaptation to the species barrier, thus poorly relevant of the real zoonotic potential of the original scrapie isolate of sheep origin49. The development of scrapie in this primate after an incubation period compatible with its lifespan complements the study conducted in transgenic (humanized) mice; taken together these studies suggest that some isolates of sheep scrapie can promote misfolding of the human prion protein and that scrapie can develop within the lifespan of some primate species.

In addition to previous studies on scrapie transmission to primate1,8,9 and the recently published study on transgenic humanized mice13, our results constitute new evidence for recommending that the potential risk of scrapie for human health should not be dismissed. Indeed, human PrP transgenic mice and primates are the most relevant models for investigating the human transmission barrier. To what extent such models are informative for measuring the zoonotic potential of an animal TSE under field exposure conditions is unknown. During the past decades, many protective measures have been successfully implemented to protect cattle from the spread of c-BSE, and some of these measures have been extended to sheep and goats to protect from scrapie according to the principle of precaution. Since cases of c-BSE have greatly reduced in number, those protective measures are currently being challenged and relaxed in the absence of other known zoonotic animal prion disease. We recommend that risk managers should be aware of the long term potential risk to human health of at least certain scrapie isolates, notably for lymphotropic strains like the classical scrapie strain used in the current study. Relatively high amounts of infectivity in peripheral lymphoid organs in animals infected with these strains could lead to contamination of food products produced for human consumption. Efforts should also be maintained to further assess the zoonotic potential of other animal prion strains in long-term studies, notably lymphotropic strains with high prevalence like CWD, which is spreading across North America, and atypical/Nor98 scrapie (Nor98)50 that was first detected in the past two decades and now represents approximately half of all reported cases of prion diseases in small ruminants worldwide, including territories previously considered as scrapie free. Even if the prevailing view is that sporadic CJD is due to the spontaneous formation of CJD prions, it remains possible that its apparent sporadic nature may, at least in part, result from our limited capacity to identify an environmental origin.


Title: Transmission of scrapie prions to primate after an extended silent incubation period) *** 

In complement to the recent demonstration that humanized mice are susceptible to scrapie, we report here the first observation of direct transmission of a natural classical scrapie isolate to a macaque after a 10-year incubation period. Neuropathologic examination revealed all of the features of a prion disease: spongiform change, neuronal loss, and accumulation of PrPres throughout the CNS. 

*** This observation strengthens the questioning of the harmlessness of scrapie to humans, at a time when protective measures for human and animal health are being dismantled and reduced as c-BSE is considered controlled and being eradicated. 

*** Our results underscore the importance of precautionary and protective measures and the necessity for long-term experimental transmission studies to assess the zoonotic potential of other animal prion strains. 


SCRAPIE WS-01: Prion diseases in animals and zoonotic potential 2016 

Prion. 10:S15-S21. 2016 ISSN: 1933-6896 printl 1933-690X online 



O.05: Transmission of prions to primates after extended silent incubation periods: Implications for BSE and scrapie risk assessment in human populations 

Emmanuel Comoy, Jacqueline Mikol, Valerie Durand, Sophie Luccantoni, Evelyne Correia, Nathalie Lescoutra, Capucine Dehen, and Jean-Philippe Deslys Atomic Energy Commission; Fontenay-aux-Roses, France 

Prion diseases (PD) are the unique neurodegenerative proteinopathies reputed to be transmissible under field conditions since decades. The transmission of Bovine Spongiform Encephalopathy (BSE) to humans evidenced that an animal PD might be zoonotic under appropriate conditions. Contrarily, in the absence of obvious (epidemiological or experimental) elements supporting a transmission or genetic predispositions, PD, like the other proteinopathies, are reputed to occur spontaneously (atpical animal prion strains, sporadic CJD summing 80% of human prion cases). Non-human primate models provided the first evidences supporting the transmissibiity of human prion strains and the zoonotic potential of BSE. Among them, cynomolgus macaques brought major information for BSE risk assessment for human health (Chen, 2014), according to their phylogenetic proximity to humans and extended lifetime. We used this model to assess the zoonotic potential of other animal PD from bovine, ovine and cervid origins even after very long silent incubation periods. 

*** We recently observed the direct transmission of a natural classical scrapie isolate to macaque after a 10-year silent incubation period, 

***with features similar to some reported for human cases of sporadic CJD, albeit requiring fourfold long incubation than BSE. Scrapie, as recently evoked in humanized mice (Cassard, 2014), 

***is the third potentially zoonotic PD (with BSE and L-type BSE), 

***thus questioning the origin of human sporadic cases. We will present an updated panorama of our different transmission studies and discuss the implications of such extended incubation periods on risk assessment of animal PD for human health. 

=============== 

***thus questioning the origin of human sporadic cases*** 

***our findings suggest that possible transmission risk of H-type BSE to sheep and human. Bioassay will be required to determine whether the PMCA products are infectious to these animals. 


Experimental transmission of the chronic wasting disease agent to swine after oral or intracranial inoculation

S. Jo Moore1,2, M. Heather West Greenlee3, Naveen Kondru3, Sireesha Manne3, Jodi D. Smith1, Robert A. Kunkle1, Anumantha Kanthasamy3 and Justin J. Greenlee1* + Author Affiliations

1Virus and Prion Research Unit, National Animal Disease Center, USDA, Agricultural Research Service, Ames, Iowa, United States of America 2Oak Ridge Institute for Science and Education, Oak Ridge, Tennessee, United States of America 3Department of Biomedical Sciences, Iowa State University College of Veterinary Medicine, Ames, Iowa, United States of America

ABSTRACT

Chronic wasting disease (CWD) is a naturally occurring, fatal neurodegenerative disease of cervids. The potential for swine to serve as a host for the agent of chronic wasting disease is unknown. The purpose of this study was to investigate the susceptibility of swine to the CWD agent following experimental oral or intracranial inoculation. Crossbred piglets were assigned to one of three groups: intracranially inoculated (n=20), orally inoculated (n=19), or non-inoculated (n=9). At approximately the age at which commercial pigs reach market weight, half of the pigs in each group were culled (‘market weight’ groups). The remaining pigs (‘aged’ groups) were allowed to incubate for up to 73 months post inoculation (MPI). Tissues collected at necropsy were examined for disease-associated prion protein (PrPSc) by western blotting (WB), antigen-capture immunoassay (EIA), immunohistochemistry (IHC) and in vitro real-time quaking induced conversion (RT-QuIC). Brain samples from selected pigs were also bioassayed in mice expressing porcine prion protein. Four intracranially inoculated aged pigs and one orally inoculated aged pig were positive by EIA, IHC and/or WB. Using RT-QuIC, PrPSc was detected in lymphoid and/or brain tissue from one or more pigs in each inoculated group. Bioassay was positive in 4 out of 5 pigs assayed. This study demonstrates that pigs can support low-level amplification of CWD prions, although the species barrier to CWD infection is relatively high. However, detection of infectivity in orally inoculated pigs using mouse bioassay raises the possibility that naturally exposed pigs could act as a reservoir of CWD infectivity.

IMPORTANCE We challenged domestic swine with the chronic wasting disease agent by inoculation directly into the brain (intracranially) or by oral gavage (orally). Disease-associated prion protein (PrPSc) was detected in brain and lymphoid tissues from intracranially and orally inoculated pigs as early as 8 months of age (6 months post-inoculation). Only one pig developed clinical neurologic signs suggestive of prion disease. The amount of PrPSc in the brains and lymphoid tissues of positive pigs was small, especially in orally inoculated pigs. Regardless, positive results in orally inoculated pigs suggest that it may be possible for swine to serve as a reservoir for prion disease under natural conditions.

FOOTNOTES

↵*Corresponding author: Email: justin.greenlee@ars.usda.gov This is a work of the U.S. Government and is not subject to copyright protection in the United States. Foreign copyrights may apply.


Research Project: TRANSMISSION, DIFFERENTIATION, AND PATHOBIOLOGY OF TRANSMISSIBLE SPONGIFORM ENCEPHALOPATHIES

Location: Virus and Prion Research

Title: Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease

Author item Moore, Sarah item Kunkle, Robert item Kondru, Naveen item Manne, Sireesha item Smith, Jodi item Kanthasamy, Anumantha item West Greenlee, M item Greenlee, Justin

Submitted to: Prion Publication Type: Abstract Only Publication Acceptance Date: 3/15/2017 Publication Date: N/A Citation: N/A Interpretive Summary:

Technical Abstract: Aims: Chronic wasting disease (CWD) is a naturally-occurring, fatal neurodegenerative disease of cervids. We previously demonstrated that disease-associated prion protein (PrPSc) can be detected in the brain and retina from pigs challenged intracranially or orally with the CWD agent. In that study, neurological signs consistent with prion disease were observed only in one pig: an intracranially challenged pig that was euthanized at 64 months post-challenge. The purpose of this study was to use an antigen-capture immunoassay (EIA) and real-time quaking-induced conversion (QuIC) to determine whether PrPSc is present in lymphoid tissues from pigs challenged with the CWD agent.

Methods: At two months of age, crossbred pigs were challenged by the intracranial route (n=20), oral route (n=19), or were left unchallenged (n=9). At approximately 6 months of age, the time at which commercial pigs reach market weight, half of the pigs in each group were culled (<6 challenge="" groups="" month="" pigs="" remaining="" the="">6 month challenge groups) were allowed to incubate for up to 73 months post challenge (mpc). The retropharyngeal lymph node (RPLN) was screened for the presence of PrPSc by EIA and immunohistochemistry (IHC). The RPLN, palatine tonsil, and mesenteric lymph node (MLN) from 6-7 pigs per challenge group were also tested using EIA and QuIC.

Results: PrPSc was not detected by EIA and IHC in any RPLNs. All tonsils and MLNs were negative by IHC, though the MLN from one pig in the oral <6 5="" 6="" at="" by="" detected="" eia.="" examined="" group="" in="" intracranial="" least="" lymphoid="" month="" months="" of="" one="" pigs="" positive="" prpsc="" quic="" the="" tissues="" was="">6 months group, 5/6 pigs in the oral <6 4="" and="" group="" months="" oral="">6 months group. Overall, the MLN was positive in 14/19 (74%) of samples examined, the RPLN in 8/18 (44%), and the tonsil in 10/25 (40%). Conclusions:

This study demonstrates that PrPSc accumulates in lymphoid tissues from pigs challenged intracranially or orally with the CWD agent, and can be detected as early as 4 months after challenge.

CWD-infected pigs rarely develop clinical disease and if they do, they do so after a long incubation period. This raises the possibility that CWD-infected pigs could shed prions into their environment long before they develop clinical disease.

Furthermore, lymphoid tissues from CWD-infected pigs could present a potential source of CWD infectivity in the animal and human food chains.


CONFIDENTIAL

EXPERIMENTAL PORCINE SPONGIFORM ENCEPHALOPATHY

While this clearly is a cause for concern we should not jump to the conclusion that this means that pigs will necessarily be infected by bone and meat meal fed by the oral route as is the case with cattle. ...


new url link; 


we cannot rule out the possibility that unrecognised subclinical spongiform encephalopathy could be present in British pigs though there is no evidence for this: only with parenteral/implantable pharmaceuticals/devices is the theoretical risk to humans of sufficient concern to consider any action.






Our records show that while some use is made of porcine materials in medicinal products, the only products which would appear to be in a hypothetically ''higher risk'' area are the adrenocorticotrophic hormone for which the source material comes from outside the United Kingdom, namely America China Sweden France and Germany. The products are manufactured by Ferring and Armour. A further product, ''Zenoderm Corium implant'' manufactured by Ethicon, makes use of porcine skin - which is not considered to be a ''high risk'' tissue, but one of its uses is described in the data sheet as ''in dural replacement''. This product is sourced from the United Kingdom..... 


new url link; 


snip...see much more here ;


WEDNESDAY, APRIL 05, 2017

Disease-associated prion protein detected in lymphoid tissues from pigs challenged with the agent of chronic wasting disease


TUESDAY, APRIL 18, 2017 

*** EXTREME USA FDA PART 589 TSE PRION FEED LOOP HOLE STILL EXIST, AND PRICE OF POKER GOES UP ***



TITLE: PATHOLOGICAL FEATURES OF CHRONIC WASTING DISEASE IN REINDEER AND DEMONSTRATION OF HORIZONTAL TRANSMISSION 


*** DECEMBER 2016 CDC EMERGING INFECTIOUS DISEASE JOURNAL CWD HORIZONTAL TRANSMISSION 


*** INFECTIOUS AGENT OF SHEEP SCRAPIE MAY PERSIST IN THE ENVIRONMENT FOR AT LEAST 16 YEARS *** 

GUDMUNDUR GEORGSSON1, SIGURDUR SIGURDARSON2 AND PAUL BROWN3 



the tse prion aka mad cow type disease is not your normal pathogen. 

The TSE prion disease survives ashing to 600 degrees celsius, that’s around 1112 degrees farenheit. 

you cannot cook the TSE prion disease out of meat. 

you can take the ash and mix it with saline and inject that ash into a mouse, and the mouse will go down with TSE. 

Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production as well. 

the TSE prion agent also survives Simulated Wastewater Treatment Processes. 

IN fact, you should also know that the TSE Prion agent will survive in the environment for years, if not decades. 

you can bury it and it will not go away. 

The TSE agent is capable of infected your water table i.e. Detection of protease-resistant cervid prion protein in water from a CWD-endemic area. 

it’s not your ordinary pathogen you can just cook it out and be done with. 

that’s what’s so worrisome about Iatrogenic mode of transmission, a simple autoclave will not kill this TSE prion agent.


1: J Neurol Neurosurg Psychiatry 1994 Jun;57(6):757-8 

Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery. 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. 

Laboratory of Central Nervous System Studies, National Institute of 

Neurological Disorders and Stroke, National Institutes of Health, 

Bethesda, MD 20892. 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 

PMID: 8006664 [PubMed - indexed for MEDLINE] 



New studies on the heat resistance of hamster-adapted scrapie agent: Threshold survival after ashing at 600°C suggests an inorganic template of replication 



Prion Infected Meat-and-Bone Meal Is Still Infectious after Biodiesel Production 



Detection of protease-resistant cervid prion protein in water from a CWD-endemic area 



A Quantitative Assessment of the Amount of Prion Diverted to Category 1 Materials and Wastewater During Processing 



Rapid assessment of bovine spongiform encephalopathy prion inactivation by heat treatment in yellow grease produced in the industrial manufacturing process of meat and bone meals 



PPo4-4: 

Survival and Limited Spread of TSE Infectivity after Burial 




Using in vitro prion replication for high sensitive detection of prions and prionlike proteins and for understanding mechanisms of transmission. 
Claudio Soto Mitchell Center for Alzheimer's diseases and related Brain disorders, Department of Neurology, University of Texas Medical School at Houston. 
***Recently, we have been using PMCA to study the role of environmental prion contamination on the horizontal spreading of TSEs. These experiments have focused on the study of the interaction of prions with plants and environmentally relevant surfaces. Our results show that plants (both leaves and roots) bind tightly to prions present in brain extracts and excreta (urine and feces) and retain even small quantities of PrPSc for long periods of time. Strikingly, ingestion of prioncontaminated leaves and roots produced disease with a 100% attack rate and an incubation period not substantially longer than feeding animals directly with scrapie brain homogenate. Furthermore, plants can uptake prions from contaminated soil and transport them to different parts of the plant tissue (stem and leaves). Similarly, prions bind tightly to a variety of environmentally relevant surfaces, including stones, wood, metals, plastic, glass, cement, etc. Prion contaminated surfaces efficiently transmit prion disease when these materials were directly injected into the brain of animals and strikingly when the contaminated surfaces were just placed in the animal cage. These findings demonstrate that environmental materials can efficiently bind infectious prions and act as carriers of infectivity, suggesting that they may play an important role in the horizontal transmission of the disease. 
======================== 
Since its invention 13 years ago, PMCA has helped to answer fundamental questions of prion propagation and has broad applications in research areas including the food industry, blood bank safety and human and veterinary disease diagnosis. 
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes. 
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification 
Wednesday, December 16, 2015 
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission *** 
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years *** 
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3 
with CWD TSE Prions, I am not sure there is any absolute yet, other than what we know with transmission studies, and we know tse prion kill, and tse prion are bad. science shows to date, that indeed soil, dirt, some better than others, can act as a carrier. same with objects, farm furniture. take it with how ever many grains of salt you wish, or not. if load factor plays a role in the end formula, then everything should be on the table, in my opinion...tss
 Oral Transmissibility of Prion Disease Is Enhanced by Binding to Soil Particles
Author Summary
Transmissible spongiform encephalopathies (TSEs) are a group of incurable neurological diseases likely caused by a misfolded form of the prion protein. TSEs include scrapie in sheep, bovine spongiform encephalopathy (‘‘mad cow’’ disease) in cattle, chronic wasting disease in deer and elk, and Creutzfeldt-Jakob disease in humans. Scrapie and chronic wasting disease are unique among TSEs because they can be transmitted between animals, and the disease agents appear to persist in environments previously inhabited by infected animals. Soil has been hypothesized to act as a reservoir of infectivity and to bind the infectious agent. In the current study, we orally dosed experimental animals with a common clay mineral, montmorillonite, or whole soils laden with infectious prions, and compared the transmissibility to unbound agent. We found that prions bound to montmorillonite and whole soils remained orally infectious, and, in most cases, increased the oral transmission of disease compared to the unbound agent. The results presented in this study suggest that soil may contribute to environmental spread of TSEs by increasing the transmissibility of small amounts of infectious agent in the environment.
tse prion soil
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
The sources of dust borne prions are unknown but it seems reasonable to assume that faecal, urine, skin, parturient material and saliva-derived prions may contribute to this mobile environmental reservoir of infectivity. This work highlights a possible transmission route for scrapie within the farm environment, and this is likely to be paralleled in CWD which shows strong similarities with scrapie in terms of prion dissemination and disease transmission. The data indicate that the presence of scrapie prions in dust is likely to make the control of these diseases a considerable challenge.
>>>Particle-associated PrPTSE molecules may migrate from locations of deposition via transport processes affecting soil particles, including entrainment in and movement with air and overland flow. <<<
Fate of Prions in Soil: A Review
Christen B. Smith, Clarissa J. Booth, and Joel A. Pedersen*
Several reports have shown that prions can persist in soil for several years. Significant interest remains in developing methods that could be applied to degrade PrPTSE in naturally contaminated soils. Preliminary research suggests that serine proteases and the microbial consortia in stimulated soils and compost may partially degrade PrPTSE. Transition metal oxides in soil (viz. manganese oxide) may also mediate prion inactivation. Overall, the effect of prion attachment to soil particles on its persistence in the environment is not well understood, and additional study is needed to determine its implications on the environmental transmission of scrapie and CWD.
P.161: Prion soil binding may explain efficient horizontal CWD transmission
Conclusion. Silty clay loam exhibits highly efficient prion binding, inferring a durable environmental reservoir, and an efficient mechanism for indirect horizontal CWD transmission.
>>>Another alternative would be an absolute prohibition on the movement of deer within the state for any purpose. While this alternative would significantly reduce the potential spread of CWD, it would also have the simultaneous effect of preventing landowners and land managers from implementing popular management strategies involving the movement of deer, and would deprive deer breeders of the ability to engage in the business of buying and selling breeder deer. Therefore, this alternative was rejected because the department determined that it placed an avoidable burden on the regulated community.<<<
Wednesday, December 16, 2015
Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission
Timm Konold1*, Stephen A. C. Hawkins2, Lisa C. Thurston3, Ben C. Maddison4, Kevin C. Gough5, Anthony Duarte1 and Hugh A. Simmons1
1 Animal Sciences Unit, Animal and Plant Health Agency Weybridge, Addlestone, UK, 2 Pathology Department, Animal and Plant Health Agency Weybridge, Addlestone, UK, 3 Surveillance and Laboratory Services, Animal and Plant Health Agency Penrith, Penrith, UK, 4 ADAS UK, School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK, 5 School of Veterinary Medicine and Science, University of Nottingham, Sutton Bonington, UK
Classical scrapie is an environmentally transmissible prion disease of sheep and goats. Prions can persist and remain potentially infectious in the environment for many years and thus pose a risk of infecting animals after re-stocking. In vitro studies using serial protein misfolding cyclic amplification (sPMCA) have suggested that objects on a scrapie affected sheep farm could contribute to disease transmission. This in vivo study aimed to determine the role of field furniture (water troughs, feeding troughs, fencing, and other objects that sheep may rub against) used by a scrapie-infected sheep flock as a vector for disease transmission to scrapie-free lambs with the prion protein genotype VRQ/VRQ, which is associated with high susceptibility to classical scrapie. When the field furniture was placed in clean accommodation, sheep became infected when exposed to either a water trough (four out of five) or to objects used for rubbing (four out of seven). This field furniture had been used by the scrapie-infected flock 8 weeks earlier and had previously been shown to harbor scrapie prions by sPMCA. Sheep also became infected (20 out of 23) through exposure to contaminated field furniture placed within pasture not used by scrapie-infected sheep for 40 months, even though swabs from this furniture tested negative by PMCA. This infection rate decreased (1 out of 12) on the same paddock after replacement with clean field furniture. Twelve grazing sheep exposed to field furniture not in contact with scrapie-infected sheep for 18 months remained scrapie free. The findings of this study highlight the role of field furniture used by scrapie-infected sheep to act as a reservoir for disease re-introduction although infectivity declines considerably if the field furniture has not been in contact with scrapie-infected sheep for several months. PMCA may not be as sensitive as VRQ/VRQ sheep to test for environmental contamination.
snip...
Discussion
Classical scrapie is an environmentally transmissible disease because it has been reported in naïve, supposedly previously unexposed sheep placed in pastures formerly occupied by scrapie-infected sheep (4, 19, 20). Although the vector for disease transmission is not known, soil is likely to be an important reservoir for prions (2) where – based on studies in rodents – prions can adhere to minerals as a biologically active form (21) and remain infectious for more than 2 years (22). Similarly, chronic wasting disease (CWD) has re-occurred in mule deer housed in paddocks used by infected deer 2 years earlier, which was assumed to be through foraging and soil consumption (23).
Our study suggested that the risk of acquiring scrapie infection was greater through exposure to contaminated wooden, plastic, and metal surfaces via water or food troughs, fencing, and hurdles than through grazing. Drinking from a water trough used by the scrapie flock was sufficient to cause infection in sheep in a clean building. Exposure to fences and other objects used for rubbing also led to infection, which supported the hypothesis that skin may be a vector for disease transmission (9). The risk of these objects to cause infection was further demonstrated when 87% of 23 sheep presented with PrPSc in lymphoid tissue after grazing on one of the paddocks, which contained metal hurdles, a metal lamb creep and a water trough in contact with the scrapie flock up to 8 weeks earlier, whereas no infection had been demonstrated previously in sheep grazing on this paddock, when equipped with new fencing and field furniture. When the contaminated furniture and fencing were removed, the infection rate dropped significantly to 8% of 12 sheep, with soil of the paddock as the most likely source of infection caused by shedding of prions from the scrapie-infected sheep in this paddock up to a week earlier.
This study also indicated that the level of contamination of field furniture sufficient to cause infection was dependent on two factors: stage of incubation period and time of last use by scrapie-infected sheep. Drinking from a water trough that had been used by scrapie sheep in the predominantly pre-clinical phase did not appear to cause infection, whereas infection was shown in sheep drinking from the water trough used by scrapie sheep in the later stage of the disease. It is possible that contamination occurred through shedding of prions in saliva, which may have contaminated the surface of the water trough and subsequently the water when it was refilled. Contamination appeared to be sufficient to cause infection only if the trough was in contact with sheep that included clinical cases. Indeed, there is an increased risk of bodily fluid infectivity with disease progression in scrapie (24) and CWD (25) based on PrPSc detection by sPMCA. Although ultraviolet light and heat under natural conditions do not inactivate prions (26), furniture in contact with the scrapie flock, which was assumed to be sufficiently contaminated to cause infection, did not act as vector for disease if not used for 18 months, which suggest that the weathering process alone was sufficient to inactivate prions.
PrPSc detection by sPMCA is increasingly used as a surrogate for infectivity measurements by bioassay in sheep or mice. In this reported study, however, the levels of PrPSc present in the environment were below the limit of detection of the sPMCA method, yet were still sufficient to cause infection of in-contact animals. In the present study, the outdoor objects were removed from the infected flock 8 weeks prior to sampling and were positive by sPMCA at very low levels (2 out of 37 reactions). As this sPMCA assay also yielded 2 positive reactions out of 139 in samples from the scrapie-free farm, the sPMCA assay could not detect PrPSc on any of the objects above the background of the assay. False positive reactions with sPMCA at a low frequency associated with de novo formation of infectious prions have been reported (27, 28). This is in contrast to our previous study where we demonstrated that outdoor objects that had been in contact with the scrapie-infected flock up to 20 days prior to sampling harbored PrPSc that was detectable by sPMCA analysis [4 out of 15 reactions (12)] and was significantly more positive by the assay compared to analogous samples from the scrapie-free farm. This discrepancy could be due to the use of a different sPMCA substrate between the studies that may alter the efficiency of amplification of the environmental PrPSc. In addition, the present study had a longer timeframe between the objects being in contact with the infected flock and sampling, which may affect the levels of extractable PrPSc. Alternatively, there may be potentially patchy contamination of this furniture with PrPSc, which may have been missed by swabbing. The failure of sPMCA to detect CWD-associated PrP in saliva from clinically affected deer despite confirmation of infectivity in saliva-inoculated transgenic mice was associated with as yet unidentified inhibitors in saliva (29), and it is possible that the sensitivity of sPMCA is affected by other substances in the tested material. In addition, sampling of amplifiable PrPSc and subsequent detection by sPMCA may be more difficult from furniture exposed to weather, which is supported by the observation that PrPSc was detected by sPMCA more frequently in indoor than outdoor furniture (12). A recent experimental study has demonstrated that repeated cycles of drying and wetting of prion-contaminated soil, equivalent to what is expected under natural weathering conditions, could reduce PMCA amplification efficiency and extend the incubation period in hamsters inoculated with soil samples (30). This seems to apply also to this study even though the reduction in infectivity was more dramatic in the sPMCA assays than in the sheep model. Sheep were not kept until clinical end-point, which would have enabled us to compare incubation periods, but the lack of infection in sheep exposed to furniture that had not been in contact with scrapie sheep for a longer time period supports the hypothesis that prion degradation and subsequent loss of infectivity occurs even under natural conditions.
In conclusion, the results in the current study indicate that removal of furniture that had been in contact with scrapie-infected animals should be recommended, particularly since cleaning and decontamination may not effectively remove scrapie infectivity (31), even though infectivity declines considerably if the pasture and the field furniture have not been in contact with scrapie-infected sheep for several months. As sPMCA failed to detect PrPSc in furniture that was subjected to weathering, even though exposure led to infection in sheep, this method may not always be reliable in predicting the risk of scrapie infection through environmental contamination. These results suggest that the VRQ/VRQ sheep model may be more sensitive than sPMCA for the detection of environmentally associated scrapie, and suggest that extremely low levels of scrapie contamination are able to cause infection in susceptible sheep genotypes.
Keywords: classical scrapie, prion, transmissible spongiform encephalopathy, sheep, field furniture, reservoir, serial protein misfolding cyclic amplification
Wednesday, December 16, 2015
*** Objects in contact with classical scrapie sheep act as a reservoir for scrapie transmission ***
*** Infectious agent of sheep scrapie may persist in the environment for at least 16 years ***
Gudmundur Georgsson1, Sigurdur Sigurdarson2 and Paul Brown3

MONDAY, JUNE 12, 2017
Rethinking Major grain organizations opposition to CFIA's control zone approach to Chronic Wasting CWD TSE Prion Mad Deer Type Disease 2017?
WEDNESDAY, MAY 17, 2017
*** Chronic Wasting Disease CWD TSE Prion aka Mad Deer Disease and the Real Estate Market Land Values ***


*** The potential impact of prion diseases on human health was greatly magnified by the recognition that interspecies transfer of BSE to humans by beef ingestion resulted in vCJD. While changes in animal feed constituents and slaughter practices appear to have curtailed vCJD, there is concern that CWD of free-ranging deer and elk in the U.S. might also cross the species barrier. Thus, consuming venison could be a source of human prion disease. Whether BSE and CWD represent interspecies scrapie transfer or are newly arisen prion diseases is unknown. Therefore, the possibility of transmission of prion disease through other food animals cannot be ruled out. There is evidence that vCJD can be transmitted through blood transfusion. There is likely a pool of unknown size of asymptomatic individuals infected with vCJD, and there may be asymptomatic individuals infected with the CWD equivalent. These circumstances represent a potential threat to blood, blood products, and plasma supplies. 




THURSDAY, AUGUST 17, 2017 

*** Monitoring the occurrence of emerging forms of Creutzfeldt-Jakob disease in the United States revisited 2017

Singeltary et al



FRIDAY, AUGUST 11, 2017 

Infectivity in bone marrow from sporadic CJD patients

Bioassays in transgenic mice expressing the human prion protein revealed the presence of unexpectedly high levels of infectivity in the bone marrow from seven out of eight sCJD cases. These findings may explain the presence of blood-borne infectivity in sCJD patients. They also suggest that the distribution of prion infectivity in peripheral tissues in sCJD patients could be wider than currently believed, with potential implications for the iatrogenic transmission risk of this disease. 



THURSDAY, AUGUST 10, 2017 

Minimise transmission risk of CJD and vCJD in healthcare settings Updated 10 August 2017



*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery *** 

Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. 

Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them. 




National Prion Center could lose all funding just as concern about CWD jumping to humans rises

SATURDAY, JULY 15, 2017 

*** National Prion Center could lose all funding just as concern about CWD jumping to humans rises



BSE TSE PRION USDA OIE NEEDLESS CONFLICT



Tracking spongiform encephalopathies in North America

Xavier Bosch

Published: August 2003


Summary;

“My name is Terry S Singeltary Sr, and I live in Bacliff, Texas. I lost my mom to hvCJD (Heidenhain variant CJD) and have been searching for answers ever since. What I have found is that we have not been told the truth. CWD in deer and elk is a small portion of a much bigger problem.”

49-year-old Singeltary is one of a number of people who have remained largely unsatisfied after being told that a close relative died from a rapidly progressive dementia compatible with spontaneous Creutzfeldt-Jakob disease (CJD). So he decided to gather hundreds of documents on transmissible spongiform encephalopathies (TSE) and realised that if Britons could get variant CJD from bovine spongiform encephalopathy (BSE), Americans might get a similar disorder from chronic wasting disease (CWD) the relative of mad cow disease seen among deer and elk in the USA. Although his feverish search did not lead him to the smoking gun linking CWD to a similar disease in North American people, it did uncover a largely disappointing situation.

Singeltary was greatly demoralised at the few attempts to monitor the occurrence of CJD and CWD in the USA. Only a few states have made CJD reportable. Human and animal TSEs should be reportable nationwide and internationally, he complained in a letter to the Journal of the American Medical Association (JAMA 2003; 285: 733). "I hope that the CDC does not continue to expect us to still believe that the 85% plus of all CJD cases which are sporadic are all spontaneous, without route or source."

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA

Diagnosis and Reporting of Creutzfeldt-Jakob Disease

To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.

Terry S. Singeltary, Sr Bacliff, Tex

1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.


Until recently, CWD was thought to be confined to the wild in a small region in Colorado. But since early 2002, it has been reported in other areas, including Wisconsin, South Dakota, and the Canadian province of Saskatchewan. Indeed, the occurrence of CWD in states that were not endemic previously increased concern about a widespread outbreak and possible transmission to people and cattle.

To date, experimental studies have proven that the CWD agent can be transmitted to cattle by intracerebral inoculation and that it can cross the mucous membranes of the digestive tract to initiate infection in lymphoid tissue before invasion of the central nervous system. Yet the plausibility of CWD spreading to people has remained elusive.

Part of the problem seems to stem from the US surveillance system. CJD is only reported in those areas known to be endemic foci of CWD. Moreover, US authorities have been criticised for not having performed enough prionic tests in farm deer and elk.

Although in November last year the US Food and Drug Administration issued a directive to state public-health and agriculture officials prohibiting material from CWD-positive animals from being used as an ingredient in feed for any animal species, epidemiological control and research in the USA has been quite different from the situation in the UK and Europe regarding BSE.

"Getting data on TSEs in the USA from the government is like pulling teeth", Singeltary argues. "You get it when they want you to have it, and only what they want you to have."

Norman Foster, director of the Cognitive Disorders Clinic at the University of Michigan (Ann Arbor, MI, USA), says that "current surveillance of prion disease in people in the USA is inadequate to detect whether CWD is occurring in human beings"; adding that, "the cases that we know about are reassuring, because they do not suggest the appearance of a new variant of CJD in the USA or atypical features in patients that might be exposed to CWD. However, until we establish a system that identifies and analyses a high proportion of suspected prion disease cases we will not know for sure". The USA should develop a system modelled on that established in the UK, he points out.

Ali Samii, a neurologist at Seattle VA Medical Center who recently reported the cases of three hunters "two of whom were friends" who died from pathologically confirmed CJD, says that "at present there are insufficient data to claim transmission of CWD into humans"; adding that "[only] by asking [the questions of venison consumption and deer/elk hunting] in every case can we collect suspect cases and look into the plausibility of transmission further". Samii argues that by making both doctors and hunters more aware of the possibility of prions spreading through eating venison, doctors treating hunters with dementia can consider a possible prion disease, and doctors treating CJD patients will know to ask whether they ate venison.

CDC spokesman Ermias Belay says that the CDC "will not be investigating the [Samii] cases because there is no evidence that the men ate CWD-infected meat". He notes that although "the likelihood of CWD jumping the species barrier to infect humans cannot be ruled out 100%" and that "[we] cannot be 100% sure that CWD does not exist in humans& the data seeking evidence of CWD transmission to humans have been very limited". 




26 March 2003 

Terry S. Singeltary, retired (medically) CJD WATCH 

I lost my mother to hvCJD (Heidenhain Variant CJD). I would like to comment on the CDC's attempts to monitor the occurrence of emerging forms of CJD. Asante, Collinge et al [1] have reported that BSE transmission to the 129-methionine genotype can lead to an alternate phenotype that is indistinguishable from type 2 PrPSc, the commonest sporadic CJD. However, CJD and all human TSEs are not reportable nationally. CJD and all human TSEs must be made reportable in every state and internationally. I hope that the CDC does not continue to expect us to still believe that the 85%+ of all CJD cases which are sporadic are all spontaneous, without route/source. We have many TSEs in the USA in both animal and man. CWD in deer/elk is spreading rapidly and CWD does transmit to mink, ferret, cattle, and squirrel monkey by intracerebral inoculation. With the known incubation periods in other TSEs, oral transmission studies of CWD may take much longer. Every victim/family of CJD/TSEs should be asked about route and source of this agent. To prolong this will only spread the agent and needlessly expose others. In light of the findings of Asante and Collinge et al, there should be drastic measures to safeguard the medical and surgical arena from sporadic CJDs and all human TSEs. I only ponder how many sporadic CJDs in the USA are type 2 PrPSc? 



2 January 2000 British Medical Journal U.S. 

Scientist should be concerned with a CJD epidemic in the U.S., as well 



15 November 1999 British Medical Journal hvCJD in the USA * BSE in U.S. 



BSE TSE PRION USDA OIE NEEDLESS CONFLICT



2001 FDA CJD TSE Prion Singeltary Submission
 *** U.S.A. 50 STATE BSE MAD COW CONFERENCE CALL Jan. 9, 2001 

*** Pennsylvania 27 deer from Bedford County farm test positive for chronic wasting disease ***



THURSDAY, SEPTEMBER 21, 2017

Pennsylvania Game Commission has scheduled a series of public meetings to ensure Pennsylvanians remain informed about chronic wasting disease CWD TSE Prion



Iowa Supreme Court rules law allows quarantine of CWD deer, not land

This is very, very concerning imo. 

IF this ruling is upheld as such ;

''The Iowa Supreme Court upheld the district court ruling — saying the law gives the DNR only the authority to quarantine the deer — not the land. The ruling says if the Iowa Legislature wants to expand the quarantine powers as suggested by the DNR, then it is free to do so.''

IF a 'precedent' is set as such, by the Legislature not intervening to expand quarantine powers to the DNR for CWD TSE Prion, and the precedent is set as such that the cervid industry and land there from, once contaminated with the CWD TSE Prion, are free to repopulate, sell the land, etc, imo, this will blow the lid off any containment efforts of this damn disease CWD TSE Prion. The Iowa Supreme Court did not just pass the cwd buck down the road, the Supreme Court of Iowa just threw the whole state of Iowa under the bus at 100 MPH. what about the exposure to the other species that come across that land, and then off to some other land? this makes no sense to me, if this is set in stone and the Legislation does not stop it, and stop if fast, any containment of the cwd tse prion will be futile, imo...terry

FRIDAY, JUNE 16, 2017

Iowa Supreme Court rules law allows quarantine of CWD deer, not land



Wednesday, March 16, 2016

Wisconsin CWD sample survey 2015 confirms 290 cases of Chronic Wasting Disease TSE Prion



Wednesday, February 10, 2016

*** Wisconsin Two deer that escaped farm had chronic wasting disease CWD ***



THURSDAY, SEPTEMBER 21, 2017

TEXAS TPWD CWD mandatory check stations for Chronic Wasting Disease in the South Central, Panhandle, and Trans-Pecos areas



MONDAY, AUGUST 14, 2017

*** Texas Chronic Wasting Disease CWD TSE Prion History



THURSDAY, AUGUST 10, 2017

*** NORWAY MAKES CHANGES TO NATIONAL CHRONIC WASTING DISEASE CWD TSE PRION RULES ***



SUNDAY, AUGUST 06, 2017 

USA Chronic Wasting Disease CWD TSE Prion Emergency Response Plan Singeltary et al 



MONDAY, MAY 29, 2017 

Canada CCA optimistic over potential for revisions to OIE criteria for BSE negligible risk



THURSDAY, AUGUST 17, 2017 

JAVMA NEWS Atypical BSE found in Alabama cow September 01, 2017



THURSDAY, JULY 20, 2017 

USDA OIE Alabama Atypical L-type BASE Bovine Spongiform Encephalopathy BSE animal feeds for ruminants rule, 21 CFR 589.200



TUESDAY, SEPTEMBER 19, 2017 

USDA APHIS Notice: Animal Disease Traceability (ADT) Summary of Feedback on the ADT Program



In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells

3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ...



Evidence That Transmissible Mink Encephalopathy Results from Feeding Infected Cattle Over the next 8-10 weeks, approximately 40% of all the adult mink on the farm died from TME. snip... The rancher was a ''dead stock'' feeder using mostly (>95%) downer or dead dairy cattle... 

In Confidence - Perceptions of unconventional slow virus diseases of animals in the USA - APRIL-MAY 1989 - G A H Wells 3. Prof. A. Robertson gave a brief account of BSE. The US approach was to accord it a very low profile indeed. Dr. A Thiermann showed the picture in the ''Independent'' with cattle being incinerated and thought this was a fanatical incident to be avoided in the US at all costs. ... 



The occurrence of CWD must be viewed against the contest of the locations in which it occurred. It was an incidental and unwelcome complication of the respective wildlife research programmes. Despite its subsequent recognition as a new disease of cervids, therefore justifying direct investigation, no specific research funding was forthcoming. The USDA veiwed it as a wildlife problem and consequently not their province! ...page 26. 



*** Spraker suggested an interesting explanation for the occurrence of CWD. The deer pens at the Foot Hills Campus were built some 30-40 years ago by a Dr. Bob Davis. At or abut that time, allegedly, some scrapie work was conducted at this site. When deer were introduced to the pens they occupied ground that had previously been occupied by sheep. 


IN CONFIDENCE TRANSMISSION OF ALZHIMER TYPE PLAQUES TO PRIMATE



Alzheimer’s disease, iatrogenic, and Transmissible Spongiform Encephalopathy TSE Prion disease, that is the question ???
>>> The only tenable public line will be that "more research is required’’ <<<
>>> possibility on a transmissible prion remains open<<<
O.K., so it’s about 23 years later, so somebody please tell me, when is "more research is required’’ enough time for evaluation ?

[9. Whilst this matter is not at the moment directly concerned with the iatrogenic CJD cases from hgH, there remains a possibility of litigation here, and this presents an added complication. There are also results to be made available shortly (1) concerning a farmer with CJD who had BSE animals, (2) on the possible transmissibility of Alzheimer’s and (3) a CMO letter on prevention of iatrogenic CJD transmission in neurosurgery, all of which will serve to increase media interest.]


snip...see full Singeltary Nature comment here;
see Singeltary comments to Plos ;


Self-Propagative Replication of Ab Oligomers Suggests Potential Transmissibility in Alzheimer Disease
*** Singeltary comment PLoS ***
Alzheimer’s disease and Transmissible Spongiform Encephalopathy prion disease, Iatrogenic, what if ?
Posted by flounder on 05 Nov 2014 at 21:27 GMT

Ann N Y Acad Sci. 1982;396:131-43. 

Alzheimer's disease and transmissible virus dementia (Creutzfeldt-Jakob disease). 

Brown P, Salazar AM, Gibbs CJ Jr, Gajdusek DC. 

Abstract 

Ample justification exists on clinical, pathologic, and biologic grounds for considering a similar pathogenesis for AD and the spongiform virus encephalopathies. However, the crux of the comparison rests squarely on results of attempts to transmit AD to experimental animals, and these results have not as yet validated a common etiology. Investigations of the biologic similarities between AD and the spongiform virus encephalopathies proceed in several laboratories, and our own observation of inoculated animals will be continued in the hope that incubation periods for AD may be even longer than those of CJD. 

Sunday, November 22, 2015
*** Effect of heating on the stability of amyloid A (AA) fibrils and the intra- and cross-species transmission of AA amyloidosis Abstract
Amyloid A (AA) amyloidosis is a protein misfolding disease characterized by extracellular deposition of AA fibrils. AA fibrils are found in several tissues from food animals with AA amyloidosis. For hygienic purposes, heating is widely used to inactivate microbes in food, but it is uncertain whether heating is sufficient to inactivate AA fibrils and prevent intra- or cross-species transmission. We examined the effect of heating (at 60 °C or 100 °C) and autoclaving (at 121 °C or 135 °C) on murine and bovine AA fibrils using Western blot analysis, transmission electron microscopy (TEM), and mouse model transmission experiments. TEM revealed that a mixture of AA fibrils and amorphous aggregates appeared after heating at 100 °C, whereas autoclaving at 135 °C produced large amorphous aggregates. AA fibrils retained antigen specificity in Western blot analysis when heated at 100 °C or autoclaved at 121 °C, but not when autoclaved at 135 °C. Transmissible pathogenicity of murine and bovine AA fibrils subjected to heating (at 60 °C or 100 °C) was significantly stimulated and resulted in amyloid deposition in mice. Autoclaving of murine AA fibrils at 121 °C or 135 °C significantly decreased amyloid deposition. Moreover, amyloid deposition in mice injected with murine AA fibrils was more severe than that in mice injected with bovine AA fibrils. Bovine AA fibrils autoclaved at 121 °C or 135 °C did not induce amyloid deposition in mice. These results suggest that AA fibrils are relatively heat stable and that similar to prions, autoclaving at 135 °C is required to destroy the pathogenicity of AA fibrils. These findings may contribute to the prevention of AA fibril transmission through food materials to different animals and especially to humans.
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*** Transmission of Creutzfeldt-Jakob disease to a chimpanzee by electrodes contaminated during neurosurgery ***
Gibbs CJ Jr, Asher DM, Kobrine A, Amyx HL, Sulima MP, Gajdusek DC. Laboratory of Central Nervous System Studies, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892.
Stereotactic multicontact electrodes used to probe the cerebral cortex of a middle aged woman with progressive dementia were previously implicated in the accidental transmission of Creutzfeldt-Jakob disease (CJD) to two younger patients. The diagnoses of CJD have been confirmed for all three cases. More than two years after their last use in humans, after three cleanings and repeated sterilisation in ethanol and formaldehyde vapour, the electrodes were implanted in the cortex of a chimpanzee. Eighteen months later the animal became ill with CJD. This finding serves to re-emphasise the potential danger posed by reuse of instruments contaminated with the agents of spongiform encephalopathies, even after scrupulous attempts to clean them.
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
Singeltary, Sr et al. JAMA.2001; 285: 733-734. Vol. 285 No. 6, February 14, 2001 JAMA
Diagnosis and Reporting of Creutzfeldt-Jakob Disease
To the Editor: In their Research Letter, Dr Gibbons and colleagues1 reported that the annual US death rate due to Creutzfeldt-Jakob disease (CJD) has been stable since 1985. These estimates, however, are based only on reported cases, and do not include misdiagnosed or preclinical cases. It seems to me that misdiagnosis alone would drastically change these figures. An unknown number of persons with a diagnosis of Alzheimer disease in fact may have CJD, although only a small number of these patients receive the postmortem examination necessary to make this diagnosis. Furthermore, only a few states have made CJD reportable. Human and animal transmissible spongiform encephalopathies should be reportable nationwide and internationally.
Terry S. Singeltary, Sr Bacliff, Tex
1. Gibbons RV, Holman RC, Belay ED, Schonberger LB. Creutzfeldt-Jakob disease in the United States: 1979-1998. JAMA. 2000;284:2322-2323.



Terry S. Singeltary Sr.
Bacliff, Texas 77518
flounder9@verizon.net


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